Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29301
P. Krishna, Anbu Jayaraman, A. Nayak, Moushumi Baidya
Introduction: Alginic acid, a polysaccharide is one of the important phytochemical ingredients of brown algae, Turbinaria conoides (J. Agardh) Kutzing. T. conoides has been studied for various pharmacological activities, yet no toxicological information found in the literature therefore, preset study aimed at extraction and isolation of alginic acid and to assess the safety profile through acute and sub acute toxicity study in both male and female rats. Materials and Methods: Alginic acid was characterized through Fourier transform infrared spectroscopy, thermo gravimetric and differential scanning calorimetric analysis. In acute toxicity study, female rats received 2000 mg/kg of isolated product, at a single dose on oral administration. In subacute toxicity study, both male and female rats were given with 100, 200 and 400 mg/kg of the isolated product, orally, for a period of 28 days consecutively and behavioral changes, hematological, biochemical and histopathological investigations were verified. Results and Discussion: In acute toxicity study, no morbidity or mortality was reported with alginic acid treated animals at a dose of 2000 mg/kg. In sub-acute toxicity study, there were no treatment related abnormalities observed in hematological and biochemical parameters except, decreased red blood cell count (400 mg/kg); increased platelets (200 mg/kg) in female rats and increased levels of liver parameters (serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, gamma glutaryl transferase); lipid parameters (total cholesterol, triglycerides and blood glucose) in both male and female rats. Histopathology studies revealed a slight infiltration of cells and congestion in blood vessels in the liver; congestion of alveolar tissue in lungs with 400 mg/kg treated animals. No behavioural changes observed. Conclusion: From the obtained results it is indicated that the oral administration of alginic acid (active principle of T. conoides) did not produce any significant adverse effects in rats of both the sex. Hence, alginic acid was considered as safe to use for further therapeutic purpose.
{"title":"Toxicological Evaluation of Alginic Acid, a Polysaccharide Isolated from Turbinaria conoides (J. Agardh) Kutzing on Wistar Albino Rats","authors":"P. Krishna, Anbu Jayaraman, A. Nayak, Moushumi Baidya","doi":"10.18311/ti/2022/v29i3/29301","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29301","url":null,"abstract":"Introduction: Alginic acid, a polysaccharide is one of the important phytochemical ingredients of brown algae, Turbinaria conoides (J. Agardh) Kutzing. T. conoides has been studied for various pharmacological activities, yet no toxicological information found in the literature therefore, preset study aimed at extraction and isolation of alginic acid and to assess the safety profile through acute and sub acute toxicity study in both male and female rats. Materials and Methods: Alginic acid was characterized through Fourier transform infrared spectroscopy, thermo gravimetric and differential scanning calorimetric analysis. In acute toxicity study, female rats received 2000 mg/kg of isolated product, at a single dose on oral administration. In subacute toxicity study, both male and female rats were given with 100, 200 and 400 mg/kg of the isolated product, orally, for a period of 28 days consecutively and behavioral changes, hematological, biochemical and histopathological investigations were verified. Results and Discussion: In acute toxicity study, no morbidity or mortality was reported with alginic acid treated animals at a dose of 2000 mg/kg. In sub-acute toxicity study, there were no treatment related abnormalities observed in hematological and biochemical parameters except, decreased red blood cell count (400 mg/kg); increased platelets (200 mg/kg) in female rats and increased levels of liver parameters (serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, gamma glutaryl transferase); lipid parameters (total cholesterol, triglycerides and blood glucose) in both male and female rats. Histopathology studies revealed a slight infiltration of cells and congestion in blood vessels in the liver; congestion of alveolar tissue in lungs with 400 mg/kg treated animals. No behavioural changes observed. Conclusion: From the obtained results it is indicated that the oral administration of alginic acid (active principle of T. conoides) did not produce any significant adverse effects in rats of both the sex. Hence, alginic acid was considered as safe to use for further therapeutic purpose.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43847591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/28705
Adnan Bozalija, S. Maliqi, Pëllumb Islami, A. Iljazi, H. Islami
This paper is studied the respiratory function as a result of the impact of air pollution in the environment of the sector of exploitation of heavy minerals such Pb, Zn, Au, Ag, Bi, Cd, PM in the mines of Trepça, Kosovo. Lung function parameters are determined by Body plethysmography. Airway resistance (Raw) was recorded and Intra-Thoracic Gas Volume (ITGV) was measured and specific resistance (SRaw) and airway specific conductance (SGaw) were calculated. The research was done in two groups, the control group and the experimental one. The control group consisted of 24 healthy people, while the experimental one is made up of 52 mining workers for the exploitation of minerals in the Trepçamine, Kosovo. The results obtained from this research indicate that the mean value of specific resistance (SRaw) is significantly higher in the experimental group (p<0.01), compared to the control group (p>0.1). Also, in this study it was confirmed that smoking favors the negative effects of air contamination in the mineral exploitation sector, the changes are significant (p<0.01). Respiratory system parameters of the control group and the experimental group were measured before and after bronchoprovocation with histamine-aerosol (1 mg/ml). The differences between these two groups after provocation were statistically significant (p<0.01). Respiratory changes from air pollution with noxae in mines where metals are mined, it takes a long time for changes in respiratory function to appear. Therefore, exposure of workers to these conditions poses a risk to their health, causing bronchial reactivity, bronchial asthma or, obstructive pulmonary syndrome.
{"title":"The Reaction of Airways of Employees Working in the Environments Polluted with Heavy Metals in Mine Kosovo","authors":"Adnan Bozalija, S. Maliqi, Pëllumb Islami, A. Iljazi, H. Islami","doi":"10.18311/ti/2022/v29i3/28705","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/28705","url":null,"abstract":"This paper is studied the respiratory function as a result of the impact of air pollution in the environment of the sector of exploitation of heavy minerals such Pb, Zn, Au, Ag, Bi, Cd, PM in the mines of Trepça, Kosovo. Lung function parameters are determined by Body plethysmography. Airway resistance (Raw) was recorded and Intra-Thoracic Gas Volume (ITGV) was measured and specific resistance (SRaw) and airway specific conductance (SGaw) were calculated. The research was done in two groups, the control group and the experimental one. The control group consisted of 24 healthy people, while the experimental one is made up of 52 mining workers for the exploitation of minerals in the Trepçamine, Kosovo. The results obtained from this research indicate that the mean value of specific resistance (SRaw) is significantly higher in the experimental group (p<0.01), compared to the control group (p>0.1). Also, in this study it was confirmed that smoking favors the negative effects of air contamination in the mineral exploitation sector, the changes are significant (p<0.01). Respiratory system parameters of the control group and the experimental group were measured before and after bronchoprovocation with histamine-aerosol (1 mg/ml). The differences between these two groups after provocation were statistically significant (p<0.01). Respiratory changes from air pollution with noxae in mines where metals are mined, it takes a long time for changes in respiratory function to appear. Therefore, exposure of workers to these conditions poses a risk to their health, causing bronchial reactivity, bronchial asthma or, obstructive pulmonary syndrome.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41912715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/28352
Prince Sharma, K. Sharma, P. Chadha
The present study was conducted to investigate the genotoxic effect of Bis-Phenol A (BPA) after acute and subchronic exposure in different tissues of Channa punctata. The recovery in DNA damage was also ascertained after 30 days of cessation of exposure. Fish were exposed to different sublethal concentrations of BPA along with two controls i.e., with positive (acetone) and negative (water) controls for 96h (acute exposure) and 60 days (subchronic exposure) and after that fish were allowed to recover for 30 days in freshwater. The blood, liver, and gill tissue samples were collected at 24, 48, 72 and 96h for acute exposure and after 20, 40, and 60 days post-exposure for subchronic exposure. Exposed groups showed significantly higher DNA damage in both acute and subchronic exposure as compared to control groups. In the case of acute exposure, the highest damage was observed at 24 h of exposure followed by a decline in the value of all the parameters, while in the later hours of exposure these values further increased. On the other hand, in the case of sub-chronic exposure, the highest damage was observed after 60 days of exposure. Recovery experiment showed a decrease in the values of all the parameters studied. The result of the study clearly showed that BPA caused DNA damage in Channa punctata after acute as well as subchronic exposure.
{"title":"DNA Damage and Repair in different Tissues of Fresh Water Fish, Channa punctata after Acute and Subchronic Exposure to bisphenol A","authors":"Prince Sharma, K. Sharma, P. Chadha","doi":"10.18311/ti/2022/v29i3/28352","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/28352","url":null,"abstract":"The present study was conducted to investigate the genotoxic effect of Bis-Phenol A (BPA) after acute and subchronic exposure in different tissues of Channa punctata. The recovery in DNA damage was also ascertained after 30 days of cessation of exposure. Fish were exposed to different sublethal concentrations of BPA along with two controls i.e., with positive (acetone) and negative (water) controls for 96h (acute exposure) and 60 days (subchronic exposure) and after that fish were allowed to recover for 30 days in freshwater. The blood, liver, and gill tissue samples were collected at 24, 48, 72 and 96h for acute exposure and after 20, 40, and 60 days post-exposure for subchronic exposure. Exposed groups showed significantly higher DNA damage in both acute and subchronic exposure as compared to control groups. In the case of acute exposure, the highest damage was observed at 24 h of exposure followed by a decline in the value of all the parameters, while in the later hours of exposure these values further increased. On the other hand, in the case of sub-chronic exposure, the highest damage was observed after 60 days of exposure. Recovery experiment showed a decrease in the values of all the parameters studied. The result of the study clearly showed that BPA caused DNA damage in Channa punctata after acute as well as subchronic exposure.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47561058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29322
Sirirak Hemmaphan, N. Bordeerat
Exposure to lead (Pb) continues to be a significant worldwide problem. Pb is a highly toxic heavy metal affecting several organ systems in the body. There has been reported to have potential genotoxic properties to various cells. However, the underlying mechanisms of lead-induced toxicity are still unknown. The present study aimed to investigate the lead-induced cytotoxicity in human renal proximal tubular epithelial cells and its underlying DNA damage mechanisms. Lead exposure caused DNA damage as demonstrated by increased 8-OHdG/dG ratio in cells even at a relatively normal dose (10μg/dL). Lead also led to producing oxidative stress as characterized by increased intensity of the Reactive Oxygen Species (ROS) indicator. ROS overproduction should be the reason for lead-induced DNA damage. Therefore, the effects of Lead on ROS elimination should be the main reason for lead-induced oxidative stress in human renal proximal tubular epithelial cells. After lead acetate (PbAc) treatment, the cell viability significantly decreased in a dose-dependent manner, and the accumulation of cellular ROS was observed. 8-OHdG levels, a marker of oxidative DNA damage, were significantly increased by both acute and chronic Pb exposure. Interestingly, the mRNA expression of the 8-oxoguanine DNA glycosylase 1 (hOGG1) significantly decreased after acute and chronic exposure. In conclusion, our study provides the first evidence to demonstrate that acute and chronic Pb exposure results in the altered expression of DNA glycosylases genes indicating the impairment of DNA repair pathways and contributing to DNA damage. These findings should be useful for the more comprehensive assessment of the toxic effects of Pb.
{"title":"Reduced DNA Glycosylases Expression and Oxidative DNA Damage Induced by Lead","authors":"Sirirak Hemmaphan, N. Bordeerat","doi":"10.18311/ti/2022/v29i3/29322","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29322","url":null,"abstract":"Exposure to lead (Pb) continues to be a significant worldwide problem. Pb is a highly toxic heavy metal affecting several organ systems in the body. There has been reported to have potential genotoxic properties to various cells. However, the underlying mechanisms of lead-induced toxicity are still unknown. The present study aimed to investigate the lead-induced cytotoxicity in human renal proximal tubular epithelial cells and its underlying DNA damage mechanisms. Lead exposure caused DNA damage as demonstrated by increased 8-OHdG/dG ratio in cells even at a relatively normal dose (10μg/dL). Lead also led to producing oxidative stress as characterized by increased intensity of the Reactive Oxygen Species (ROS) indicator. ROS overproduction should be the reason for lead-induced DNA damage. Therefore, the effects of Lead on ROS elimination should be the main reason for lead-induced oxidative stress in human renal proximal tubular epithelial cells. After lead acetate (PbAc) treatment, the cell viability significantly decreased in a dose-dependent manner, and the accumulation of cellular ROS was observed. 8-OHdG levels, a marker of oxidative DNA damage, were significantly increased by both acute and chronic Pb exposure. Interestingly, the mRNA expression of the 8-oxoguanine DNA glycosylase 1 (hOGG1) significantly decreased after acute and chronic exposure. In conclusion, our study provides the first evidence to demonstrate that acute and chronic Pb exposure results in the altered expression of DNA glycosylases genes indicating the impairment of DNA repair pathways and contributing to DNA damage. These findings should be useful for the more comprehensive assessment of the toxic effects of Pb.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44212410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29153
Vijetha Pendyala, S. Thakur, Lavanya Yadikar, Manga Devi Chinta
Chrysin (5,7-dihydroxyflavone) is a flavonoid with a vast number of pharmacological properties because of its antioxidant potential. Chronic stress is one of the predominant etiological factors which evoke molecular alterations in the brain leading to the development of depressive disorder. In the present study, we investigated the effect of Chrysin on Chronic Unpredictable Mild Stress (CUMS) induced alterations in behavior, noradrenergic as well as serotonergic function, and inflammation in brain. Randomly, mice were divided into four groups of six animals in each group. On 28th day after assessing behavioral parameters, brain biochemical markers were assessed. From the results, it is concluded that the chrysin protects the brain cells from CUMS induced molecular changes by attenuation of inflammation and oxidative stress.
{"title":"Chrysin Attenuates Chronic Unpredictable Mild Stress Induced Changes in Behavior, Inflammation and Improves Adrenergic, Serotonergic Function: An In-vivo and Biochemical Study","authors":"Vijetha Pendyala, S. Thakur, Lavanya Yadikar, Manga Devi Chinta","doi":"10.18311/ti/2022/v29i3/29153","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29153","url":null,"abstract":"Chrysin (5,7-dihydroxyflavone) is a flavonoid with a vast number of pharmacological properties because of its antioxidant potential. Chronic stress is one of the predominant etiological factors which evoke molecular alterations in the brain leading to the development of depressive disorder. In the present study, we investigated the effect of Chrysin on Chronic Unpredictable Mild Stress (CUMS) induced alterations in behavior, noradrenergic as well as serotonergic function, and inflammation in brain. Randomly, mice were divided into four groups of six animals in each group. On 28th day after assessing behavioral parameters, brain biochemical markers were assessed. From the results, it is concluded that the chrysin protects the brain cells from CUMS induced molecular changes by attenuation of inflammation and oxidative stress.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44317257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29822
Maitrayee Banerjee, Oly Banerjee, Siddharth Singh, S. Mukherjee
With the agricultural expansion the use of pesticides is increasing rapidly in developing countries. Endosulfan, an organochlorine insecticide, is a broadspectrum effective compound used in wide variety of agricultural crops but known to generate free radicals in the liver and caused hepatotoxicity. Thus, we considered it necessary to explore the protective effect of black tea extract against endusulfan mediated hepatotoxicity. 18 male albino Wistar rats were divided into 3 groups: Control, endosulfan treated (5mg/kg body weight/day) and endosulfan+black tea extract treated (1ml of 2.5gm%/100gm of body weight/day). After 30 days of treatment period, all the animals were sacrificed, and blood and liver tissue were collected. Serum and tissue cholesterol, serum liver function parameters, liver oxidative stress parameters and serum proinflammatory cytokines were measured. Liver sections were stained with haematoxylene and eosine and histological evaluation was done. Results revealed that endusulfan induces oxidative stress in liver by altering oxidant/antioxidant balance, and causes inflammation resulting into hepatic damage. Black tea extract supplementation shows considerable protection against endosulfan mediated changes in liver. Thus, black tea extract exerts ameliorative effect against endosulfan mediated liver toxicity.
{"title":"Protective Effects of Black Tea (Camellia sinensis) Extract on Endosulfan Induced Oxidative Stress, Inflammation and Hepatic Damage in Rats","authors":"Maitrayee Banerjee, Oly Banerjee, Siddharth Singh, S. Mukherjee","doi":"10.18311/ti/2022/v29i3/29822","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29822","url":null,"abstract":"With the agricultural expansion the use of pesticides is increasing rapidly in developing countries. Endosulfan, an organochlorine insecticide, is a broadspectrum effective compound used in wide variety of agricultural crops but known to generate free radicals in the liver and caused hepatotoxicity. Thus, we considered it necessary to explore the protective effect of black tea extract against endusulfan mediated hepatotoxicity. 18 male albino Wistar rats were divided into 3 groups: Control, endosulfan treated (5mg/kg body weight/day) and endosulfan+black tea extract treated (1ml of 2.5gm%/100gm of body weight/day). After 30 days of treatment period, all the animals were sacrificed, and blood and liver tissue were collected. Serum and tissue cholesterol, serum liver function parameters, liver oxidative stress parameters and serum proinflammatory cytokines were measured. Liver sections were stained with haematoxylene and eosine and histological evaluation was done. Results revealed that endusulfan induces oxidative stress in liver by altering oxidant/antioxidant balance, and causes inflammation resulting into hepatic damage. Black tea extract supplementation shows considerable protection against endosulfan mediated changes in liver. Thus, black tea extract exerts ameliorative effect against endosulfan mediated liver toxicity.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47518986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29893
J. Aprioku, Yabari Richard Asa
Mancozeb is a dithiocarbamate fungicide used effectively to protect plant products against fungi. The hepatic effects of short term exposure to mancozeb in adult male Wistar rats were investigated in the present study. Twenty-four animals were divided into four equal groups. Two groups were administered mancozeb (60 mg/kg body weight as single dose or 30 mg/kg body weight daily for 10 days, intraperitoneally), and the others, which served as control groups, received normal saline. Liver biochemical parameters in plasma were measured using standard methods. Liver homogenates were analysed for oxidative stress biomarkers and liver histopathology was studied. Single dose and 10 days exposures of mancozeb caused elevation in the activities of Alanine Transaminase (ALT), Aspartate Transaminase (AST), Alkaline Phosphatase (ALP), Lactate Dehydrogenase (LDH), and Gamma Glutamyl Transpeptidase (GGT) in plasma (p<0.05-0.001) compared with control. Mancozeb also caused elevation in the plasma level of total bilirubin, and reductions in albumin, total protein, and conjugated bilirubin. In addition, Malondialdehyde (MDA) and Advanced Oxidation Protein Product (AOPP) levels were increased in hepatic tissues (p<0.001) of all mancozeb exposed rats. Furthermore, hepatic levels of protein, reduced Glutathione (GSH) and vitamin C were decreased (p<0.01), together with the activities of Superoxide Dismutase (SOD), catalase, and Glutathione Peroxidase (GPx) enzymes (p<0.01-0.001). Histological analysis showed severe histopathological changes in mancozeb exposed rats. The results demonstrated that single dose intraperitoneal exposure of mancozeb (60 mg/kg body weight) or short term (10 days) daily exposure at 30 mg/kg body weight is capable of causing hepatotoxic effects in rats.
{"title":"Hepatotoxicity of Short Term Exposure to Mancozeb Fungicide in Male Wistar Rats","authors":"J. Aprioku, Yabari Richard Asa","doi":"10.18311/ti/2022/v29i3/29893","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29893","url":null,"abstract":"Mancozeb is a dithiocarbamate fungicide used effectively to protect plant products against fungi. The hepatic effects of short term exposure to mancozeb in adult male Wistar rats were investigated in the present study. Twenty-four animals were divided into four equal groups. Two groups were administered mancozeb (60 mg/kg body weight as single dose or 30 mg/kg body weight daily for 10 days, intraperitoneally), and the others, which served as control groups, received normal saline. Liver biochemical parameters in plasma were measured using standard methods. Liver homogenates were analysed for oxidative stress biomarkers and liver histopathology was studied. Single dose and 10 days exposures of mancozeb caused elevation in the activities of Alanine Transaminase (ALT), Aspartate Transaminase (AST), Alkaline Phosphatase (ALP), Lactate Dehydrogenase (LDH), and Gamma Glutamyl Transpeptidase (GGT) in plasma (p<0.05-0.001) compared with control. Mancozeb also caused elevation in the plasma level of total bilirubin, and reductions in albumin, total protein, and conjugated bilirubin. In addition, Malondialdehyde (MDA) and Advanced Oxidation Protein Product (AOPP) levels were increased in hepatic tissues (p<0.001) of all mancozeb exposed rats. Furthermore, hepatic levels of protein, reduced Glutathione (GSH) and vitamin C were decreased (p<0.01), together with the activities of Superoxide Dismutase (SOD), catalase, and Glutathione Peroxidase (GPx) enzymes (p<0.01-0.001). Histological analysis showed severe histopathological changes in mancozeb exposed rats. The results demonstrated that single dose intraperitoneal exposure of mancozeb (60 mg/kg body weight) or short term (10 days) daily exposure at 30 mg/kg body weight is capable of causing hepatotoxic effects in rats.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42941794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29732
Ammar A. Mohammed, F. Mohammad
Diphenhydramine antagonizes poisoning produced by cholinesterase (ChE) inhibiting insecticides. This study examines the effects of diphenhydramine against acute poisoning induced by the carbamate insecticide carbaryl in a chick model. The effects of diphenhydramine on the 24 h median Lethal Dose (LD50), and acute toxicity of carbaryl were assessed in chicks (7-15 days old). The plasma and whole brain ChE activities were measured electrometrically in vitro and in vivo. Diphenhydramine at 10mg/Kg Body wt. administered intramuscularly 15 min before carbaryl dosing increased the oral LD50 value of carbaryl (207 mg/Kg Body wt.) by 62%. Carbaryl at 250 mg/Kg Body wt. has orally produced toxidrome of cholinergic poisoning with 100% lethality in 24 h. Diphenhydramine (10mg/ Kg Body wt.) used 15 min before carbaryl (250mg/Kg Body wt., orally) was the most effective dose (vs 5 and 20mg/Kg Body wt.) in delaying carbaryl-toxicity and increasing survivals in chicks. The intramuscular median effective dose (ED50) of diphenhydramine which prevented 24 h carbaryl-death in chicks was 8.6mg/ Kg Body wt. The antidotal response to diphenhydramine was similar to that of the standard antidote atropine sulfate. Diphenhydramine at 10mg/Kg Body wt., given immediately after carbaryl (200mg/Kg Body wt.), reduced the percentages of plasma and whole brain ChE inhibitions in vivo by 12- and 13%, respectively. Carbaryl (10μmol/L) in vitro inhibited ChE activities in the plasma and brain by 53 and 77%, respectively; these inhibitions were reduced by 13- and 14%, respectively, when diphenhydramine (10μmol/L) was added to in vitro reactions. Diphenhydramine exerted antidotal action against a model of acute and lethal carbaryl intoxication in chicks.
{"title":"Recognition and Assessment of Antidotal Effects of Diphenhydramine against Acute Carbaryl Insecticide Poisoning in a Chick Model","authors":"Ammar A. Mohammed, F. Mohammad","doi":"10.18311/ti/2022/v29i3/29732","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29732","url":null,"abstract":"Diphenhydramine antagonizes poisoning produced by cholinesterase (ChE) inhibiting insecticides. This study examines the effects of diphenhydramine against acute poisoning induced by the carbamate insecticide carbaryl in a chick model. The effects of diphenhydramine on the 24 h median Lethal Dose (LD50), and acute toxicity of carbaryl were assessed in chicks (7-15 days old). The plasma and whole brain ChE activities were measured electrometrically in vitro and in vivo. Diphenhydramine at 10mg/Kg Body wt. administered intramuscularly 15 min before carbaryl dosing increased the oral LD50 value of carbaryl (207 mg/Kg Body wt.) by 62%. Carbaryl at 250 mg/Kg Body wt. has orally produced toxidrome of cholinergic poisoning with 100% lethality in 24 h. Diphenhydramine (10mg/ Kg Body wt.) used 15 min before carbaryl (250mg/Kg Body wt., orally) was the most effective dose (vs 5 and 20mg/Kg Body wt.) in delaying carbaryl-toxicity and increasing survivals in chicks. The intramuscular median effective dose (ED50) of diphenhydramine which prevented 24 h carbaryl-death in chicks was 8.6mg/ Kg Body wt. The antidotal response to diphenhydramine was similar to that of the standard antidote atropine sulfate. Diphenhydramine at 10mg/Kg Body wt., given immediately after carbaryl (200mg/Kg Body wt.), reduced the percentages of plasma and whole brain ChE inhibitions in vivo by 12- and 13%, respectively. Carbaryl (10μmol/L) in vitro inhibited ChE activities in the plasma and brain by 53 and 77%, respectively; these inhibitions were reduced by 13- and 14%, respectively, when diphenhydramine (10μmol/L) was added to in vitro reactions. Diphenhydramine exerted antidotal action against a model of acute and lethal carbaryl intoxication in chicks.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41739113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/30342
N. Nithyashree, N. Prakash, Prashantkumar Waghe, C. Santhosh, B. Pavithra, R. Rajashekaraiah, M. Sathyanarayana, U. Sunilchandra, K. R. Anjan Kumar, S. Manjunatha, Y. Muralidhar, G. Shivaprasad
The present study was carried out to examine the ameliorative potential of nanocurcumin against arsenic induced (sub-chronic) alterations in central nervous system in male Wistar rats. Nanocurcumin was synthesised and the hydrodynamic diameter, zeta potential and particle size were~76.60 nm, (-) 30 mV and 95nm, respectively. Experimental rats sub-chronically exposed to sodium (meta) arsenite (As; 10 mg.kg-1; 70 days; p.o) induced significant (p<0.05) reduction in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione and favoured free radical generation and induced lipid peroxidation in brain tissue. The exposure resulted in significant (p<0.05) decrease in voluntary- and involuntary motor activities and enhanced anxiety levels. However, experimental rats receiving nanocurcumin (15 mg.kg-1; p.o) showed significant (p<0.05) recovery in enzymatic - and non-enzymatic antioxidant defence system and restoration of redox balance and overcome arsenic induced depression in motor activities and elevated anxiety levels. Further, Arsenic induced elevation in pro-inflammatory cytokines, cyclooxygenase-2 activity and prostaglandin-E2 in brain and angiotensin-II levels (plasma) was significantly (p<0.05) ameliorated by nanocurcumin. Additionally, quantitative real -time polymerase chain reaction revealed a fivefold decrease in Nox2 expression in brain following nanocurcumin administration. Thus, the study concludes that nanocurcumin can serve as a potential therapeutic candidate to counter arsenic induced redox imbalance and neuropharmacological disturbances and there exists a vast scope to exploit its utility after appropriate clinical modelling.
{"title":"Nanocurcumin Restores Arsenic-Induced Disturbances in Neuropharmacological Activities in Wistar Rats","authors":"N. Nithyashree, N. Prakash, Prashantkumar Waghe, C. Santhosh, B. Pavithra, R. Rajashekaraiah, M. Sathyanarayana, U. Sunilchandra, K. R. Anjan Kumar, S. Manjunatha, Y. Muralidhar, G. Shivaprasad","doi":"10.18311/ti/2022/v29i3/30342","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/30342","url":null,"abstract":"The present study was carried out to examine the ameliorative potential of nanocurcumin against arsenic induced (sub-chronic) alterations in central nervous system in male Wistar rats. Nanocurcumin was synthesised and the hydrodynamic diameter, zeta potential and particle size were~76.60 nm, (-) 30 mV and 95nm, respectively. Experimental rats sub-chronically exposed to sodium (meta) arsenite (As; 10 mg.kg-1; 70 days; p.o) induced significant (p<0.05) reduction in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione and favoured free radical generation and induced lipid peroxidation in brain tissue. The exposure resulted in significant (p<0.05) decrease in voluntary- and involuntary motor activities and enhanced anxiety levels. However, experimental rats receiving nanocurcumin (15 mg.kg-1; p.o) showed significant (p<0.05) recovery in enzymatic - and non-enzymatic antioxidant defence system and restoration of redox balance and overcome arsenic induced depression in motor activities and elevated anxiety levels. Further, Arsenic induced elevation in pro-inflammatory cytokines, cyclooxygenase-2 activity and prostaglandin-E2 in brain and angiotensin-II levels (plasma) was significantly (p<0.05) ameliorated by nanocurcumin. Additionally, quantitative real -time polymerase chain reaction revealed a fivefold decrease in Nox2 expression in brain following nanocurcumin administration. Thus, the study concludes that nanocurcumin can serve as a potential therapeutic candidate to counter arsenic induced redox imbalance and neuropharmacological disturbances and there exists a vast scope to exploit its utility after appropriate clinical modelling.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42221240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-12DOI: 10.18311/ti/2022/v29i3/29790
Rojison Koshy, D. Narayana, S. Yadav, Vineet Kumar Singh, Deepak Mundkinajeddu
History of safe use, HoSU preparations are formulations mentioned in ancient literature and are according to the Ayurvedic system of medicine. Due to the advent of new technologies, there is a shift in the manufacturing methodologies of Ayurvedic medicines involving extractions and fractionations. This shift, while has helped manufacturers improve their productivity, raises a question on the equivalence to chemistry, and toxicity when compared to traditional products. As a case study, an attempt is made to establish equivalence between HoSU preparation of Terminalia chebula with commercially available aqueous and alcoholic extracts and one of its fractions. Chemical analysis of the products using principal component analysis, revealed similar chemistry whereas the LC50 values of HoSU preparation were safest followed by commercial preparations and the reference marker compound when tested on zebrafish. The generated data indicated that chemical composition of all 4 samples tested were similar qualitatively, though variations were observed quantitatively. PCA plot indicated that the HoSU extract, commercial alcoholic extract, and commercial water extract were similar whereas water acetone extract was dissimilar. This emphasizes the need for conducting an equivalence study in terms of chemistry and toxicity between HoSU products and commercially available products.
{"title":"Comparison of Chemistry and Zebrafish Toxicological Profile of Extract Processed as Per Traditional Method and of its Fraction for Similarity/Dissimilarity – A Case Study of Terminalia chebula Fruit","authors":"Rojison Koshy, D. Narayana, S. Yadav, Vineet Kumar Singh, Deepak Mundkinajeddu","doi":"10.18311/ti/2022/v29i3/29790","DOIUrl":"https://doi.org/10.18311/ti/2022/v29i3/29790","url":null,"abstract":"History of safe use, HoSU preparations are formulations mentioned in ancient literature and are according to the Ayurvedic system of medicine. Due to the advent of new technologies, there is a shift in the manufacturing methodologies of Ayurvedic medicines involving extractions and fractionations. This shift, while has helped manufacturers improve their productivity, raises a question on the equivalence to chemistry, and toxicity when compared to traditional products. As a case study, an attempt is made to establish equivalence between HoSU preparation of Terminalia chebula with commercially available aqueous and alcoholic extracts and one of its fractions. Chemical analysis of the products using principal component analysis, revealed similar chemistry whereas the LC50 values of HoSU preparation were safest followed by commercial preparations and the reference marker compound when tested on zebrafish. The generated data indicated that chemical composition of all 4 samples tested were similar qualitatively, though variations were observed quantitatively. PCA plot indicated that the HoSU extract, commercial alcoholic extract, and commercial water extract were similar whereas water acetone extract was dissimilar. This emphasizes the need for conducting an equivalence study in terms of chemistry and toxicity between HoSU products and commercially available products.","PeriodicalId":23205,"journal":{"name":"Toxicology International","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67530838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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