Pub Date : 2022-01-01Epub Date: 2022-04-21DOI: 10.1186/s42269-022-00798-w
Abdus Salam Raju, Aditya Thomas Benjamin, Tristan Rutland, Luke Liu, Paul Lambrakis
Background: Vasculitis and phlebitis with vascular occlusion within appendix specimen is rare. Several authors have reported COVID-19 related veno-occlusive disease in hepatic pathology, but lymphoid aggregation with phlebitis is unusual in appendix specimen. We present a case with medium size venule phlebitis in an appendix of a patient recovered from COVID-19 infection.
Case presentation: A 27-year-old who recently recovered from COVID-19 infection 12 weeks prior, presented with acute appendicitis, confirmed on computed tomography and operative findings. He underwent an uneventful laparoscopic appendicectomy. Histopathology showed veno-occlusive vasculitis within the appendix specimen.
Conclusions: Veno-occlusive disease within the appendix is uncommon. Emerging data suggest COVID-19 infection can cause systemic vascular complications. We herein report a case of healthy patient with no past medical history with an unusual findings of medium vessels phlebitis within the appendix post COVID-19 infection.
{"title":"Appendicitis and COVID: cause or effect?","authors":"Abdus Salam Raju, Aditya Thomas Benjamin, Tristan Rutland, Luke Liu, Paul Lambrakis","doi":"10.1186/s42269-022-00798-w","DOIUrl":"10.1186/s42269-022-00798-w","url":null,"abstract":"<p><strong>Background: </strong>Vasculitis and phlebitis with vascular occlusion within appendix specimen is rare. Several authors have reported COVID-19 related veno-occlusive disease in hepatic pathology, but lymphoid aggregation with phlebitis is unusual in appendix specimen. We present a case with medium size venule phlebitis in an appendix of a patient recovered from COVID-19 infection.</p><p><strong>Case presentation: </strong>A 27-year-old who recently recovered from COVID-19 infection 12 weeks prior, presented with acute appendicitis, confirmed on computed tomography and operative findings. He underwent an uneventful laparoscopic appendicectomy. Histopathology showed veno-occlusive vasculitis within the appendix specimen.</p><p><strong>Conclusions: </strong>Veno-occlusive disease within the appendix is uncommon. Emerging data suggest COVID-19 infection can cause systemic vascular complications. We herein report a case of healthy patient with no past medical history with an unusual findings of medium vessels phlebitis within the appendix post COVID-19 infection.</p>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"57 1","pages":"114"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9021817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75423832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stefan Müller-Lissner, Gabrio Bassotti, Benoit Coffin, Asbjørn Mohr Drewes, Harald Breivik, Elon Eisenberg, Anton Emmanuel, Françoise Laroche, Winfried Meissner, Bart Morlion
Objective: To formulate timely evidence-based guidelines for the management of opioid-induced bowel dysfunction.
Setting: Constipation is a major untoward effect of opioids. Increasing prescription of opioids has correlated to increased incidence of opioid-induced constipation. However, the inhibitory effects of opioids are not confined to the colon, but also affect higher segments of the gastrointestinal tract, leading to the coining of the term "opioid-induced bowel dysfunction."
Methods: A literature search was conducted using Medline, EMBASE, and EMBASE Classic, and the Cochrane Central Register of Controlled Trials. Predefined search terms and inclusion/exclusion criteria were used to identify and categorize relevant papers. A series of statements were formulated and justified by a comment, then labeled with the degree of agreement and their level of evidence as judged by the Strength of Recommendation Taxonomy (SORT) system.
Results: From a list of 10,832 potentially relevant studies, 33 citations were identified for review. Screening the reference lists of the pertinent papers identified additional publications. Current definitions, prevalence, and mechanism of opioid-induced bowel dysfunction were reviewed, and a treatment algorithm and statements regarding patient management were developed to provide guidance on clinical best practice in the management of patients with opioid-induced constipation and opioid-induced bowel dysfunction.
Conclusions: In recent years, more insight has been gained in the pathophysiology of this "entity"; new treatment approaches have been developed, but guidelines on clinical best practice are still lacking. Current knowledge is insufficient regarding management of the opioid side effects on the upper gastrointestinal tract, but recommendations can be derived from what we know at present.
目的针对阿片类药物引起的肠道功能紊乱，及时制定循证管理指南：便秘是阿片类药物的主要不良反应。阿片类药物处方量的增加与阿片类药物引起的便秘发生率增加有关。然而，阿片类药物的抑制作用并不局限于结肠，还会影响胃肠道的更高部位，因此被称为 "阿片类药物引起的肠道功能紊乱"：使用 Medline、EMBASE、EMBASE Classic 和 Cochrane Central Register of Controlled Trials 进行文献检索。使用预定义的检索词和纳入/排除标准对相关论文进行识别和分类。然后，根据推荐强度分类法（SORT）系统的判断，制定了一系列声明并通过评论加以说明，然后标注同意程度及其证据级别：从 10,832 项可能相关的研究中，确定了 33 项引文供审查。对相关论文的参考文献目录进行筛选后，还发现了其他出版物。对阿片类药物引起的肠道功能紊乱的当前定义、发病率和机制进行了回顾，并制定了治疗算法和患者管理声明，为阿片类药物引起的便秘和阿片类药物引起的肠道功能紊乱患者的临床最佳治疗方法提供指导：结论：近年来，人们对这一 "实体 "的病理生理学有了更深入的了解；开发了新的治疗方法，但仍缺乏临床最佳实践指南。目前关于阿片类药物对上消化道副作用的管理知识还不够充分，但可以从我们目前所知的知识中得出一些建议。
{"title":"Opioid-Induced Constipation and Bowel Dysfunction: A Clinical Guideline.","authors":"Stefan Müller-Lissner, Gabrio Bassotti, Benoit Coffin, Asbjørn Mohr Drewes, Harald Breivik, Elon Eisenberg, Anton Emmanuel, Françoise Laroche, Winfried Meissner, Bart Morlion","doi":"10.1093/pm/pnw255","DOIUrl":"10.1093/pm/pnw255","url":null,"abstract":"<p><strong>Objective: </strong>To formulate timely evidence-based guidelines for the management of opioid-induced bowel dysfunction.</p><p><strong>Setting: </strong>Constipation is a major untoward effect of opioids. Increasing prescription of opioids has correlated to increased incidence of opioid-induced constipation. However, the inhibitory effects of opioids are not confined to the colon, but also affect higher segments of the gastrointestinal tract, leading to the coining of the term \"opioid-induced bowel dysfunction.\"</p><p><strong>Methods: </strong>A literature search was conducted using Medline, EMBASE, and EMBASE Classic, and the Cochrane Central Register of Controlled Trials. Predefined search terms and inclusion/exclusion criteria were used to identify and categorize relevant papers. A series of statements were formulated and justified by a comment, then labeled with the degree of agreement and their level of evidence as judged by the Strength of Recommendation Taxonomy (SORT) system.</p><p><strong>Results: </strong>From a list of 10,832 potentially relevant studies, 33 citations were identified for review. Screening the reference lists of the pertinent papers identified additional publications. Current definitions, prevalence, and mechanism of opioid-induced bowel dysfunction were reviewed, and a treatment algorithm and statements regarding patient management were developed to provide guidance on clinical best practice in the management of patients with opioid-induced constipation and opioid-induced bowel dysfunction.</p><p><strong>Conclusions: </strong>In recent years, more insight has been gained in the pathophysiology of this \"entity\"; new treatment approaches have been developed, but guidelines on clinical best practice are still lacking. Current knowledge is insufficient regarding management of the opioid side effects on the upper gastrointestinal tract, but recommendations can be derived from what we know at present.</p>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"96 1","pages":"1837-1863"},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5914368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75621271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1993-07-01DOI: 10.1016/0742-8413(93)90082-V
Naofumi Kitabatake, Etsushiro Doi, Alka B. Trivedi
1. The cytotoxicities of the nephrotoxic mycotoxins, citrinin and ochratoxin A were assayed on HeLa, C3H/10T1/2, NIH/3T3, MDCK (canine kidney), and HeLa P3 cell lines, using the MTT colorimetric assay.
2. Citrinin was less toxic than ochratoxin A in all of the cell lines examined.
3. The MDCK cells were more susceptible to both citrinin and ochratoxin A, in comparison with other cell lines.
4. Dose-responses, as measured by activities of leucine aminopeptidase and alkaline phosphatase of MDCK cells, were less sensitive than MTT colorimetric assay, indicating that these enzymes were not specifically inhibited in MDCK cells.
5. The ld50 of both toxins, calculated at 72 hr of incubation, was in the same order as those reported from animal experiments using rats and mice.
{"title":"Toxicity evaluation of the mycotoxins, citrinin and ochratoxin a, using several animal cell lines","authors":"Naofumi Kitabatake, Etsushiro Doi, Alka B. Trivedi","doi":"10.1016/0742-8413(93)90082-V","DOIUrl":"10.1016/0742-8413(93)90082-V","url":null,"abstract":"<div><p>1. The cytotoxicities of the nephrotoxic mycotoxins, citrinin and ochratoxin A were assayed on HeLa, C3H/10T1/2, NIH/3T3, MDCK (canine kidney), and HeLa P3 cell lines, using the MTT colorimetric assay.</p><p>2. Citrinin was less toxic than ochratoxin A in all of the cell lines examined.</p><p>3. The MDCK cells were more susceptible to both citrinin and ochratoxin A, in comparison with other cell lines.</p><p>4. Dose-responses, as measured by activities of leucine aminopeptidase and alkaline phosphatase of MDCK cells, were less sensitive than MTT colorimetric assay, indicating that these enzymes were not specifically inhibited in MDCK cells.</p><p>5. The <span>ld</span><sub>50</sub> of both toxins, calculated at 72 hr of incubation, was in the same order as those reported from animal experiments using rats and mice.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 429-433"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90082-V","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901040","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 : 1993-07-01DOI: 10.1016/0742-8413(93)90096-4
M. Bagchi, E. Hassoun, P. Akubue, D. Bagchi, S.J. Stohs
1. Endrin is a polyhalogenated cyclic hydrocarbon which produces hepatic and neurologic toxicity. In order to further assess the mechanism of toxicity ofendrin, the dose-dependent effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide (NO) production by peritoneal exudate cells (primarily macrophages) were investigated in C57BL/6J and DBA/2 mice which vary at the Ah receptor genetic locus. C57BL/6J mice are dioxin-responsive, while DBA/2 mice are dioxin-insensitive.
2. Mice of both strains were treated with 0, 1, 2 or 4 mg endrin kg−1 as a single oral dose in corn oil, and the animals were killed 24 hr post-treatment. At doses of 1,2 and 4 mg endrin kg−1 in C57BL/6J mice, hepatic mitochondrial lipid peroxidation increased 1.2-, 2.2- and 3.2-fold, respectively, and 1.8-, 2.3- and 3.5-fold with microsomes, respectively. At these same doses in DBA/2 mice, hepatic mitochondrial lipid peroxidation increased 1.3-, 2.0- and 2.6-fold, respectively, and 1.5-, 1.9- and 2.5-fold with microsomes, respectively.
3. Increases of 2.3-, 2.4- and 4.9-fold were observed in hepatic DNA damage (elution constants) in C57BL/6J mice at doses of 1, 2 and 4 mg endrin kg−1, respectively, while at these same three doses, increases of 1.9-, 2.1- and 2.3-fold were observed for DBA/2 mice, respectively.
4. Nitric oxide production by peritoneal macrophages from C57BL/6J increased by 1.3-, 1.7- and 2.0-fold with doses of 1, 2 and 4 mg endrin kg−1, respectively, while in macrophages from DBA/2 mice at these same doses, increases of 1.7-, 1.7- and 1.8-fold, respectively, were observed.
5. The results indicate that the responsiveness of peritoneal macrophages with respect to both DNA damage and nitric oxide production are more dose-dependent in C57BL/6J mice as compared to DBA/2 mice, while similar results are observed with the lipid peroxidation of hepatic mitochondria and microsomes of the two mouse strains. The results suggest that the toxicity of endrin is less reliant on a mechanism which may involve the Ah receptor system as compared to dioxins as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
1. Endrin是一种多卤环烃，具有肝脏和神经毒性。为了进一步研究endrin的毒性机制，我们在Ah受体基因位点不同的C57BL/6J和DBA/2小鼠中研究了endrin对肝脂质过氧化和DNA损伤以及腹腔渗出细胞(主要是巨噬细胞)产生一氧化氮(NO)的剂量依赖性作用。C57BL/6J小鼠对二恶英有反应，DBA/2小鼠对二恶英无反应。用0、1、2或4 mg endrin kg - 1单次灌胃玉米油，24小时后处死小鼠。C57BL/6J小鼠在1、2和4 mg endrin kg - 1剂量下，肝脏线粒体脂质过氧化分别增加1.2倍、2.2倍和3.2倍，微粒体分别增加1.8倍、2.3倍和3.5倍。在相同剂量的DBA/2小鼠中，肝脏线粒体脂质过氧化分别增加1.3倍，2.0倍和2.6倍，微粒体分别增加1.5倍，1.9倍和2.5倍。在1、2和4 mg endrin kg - 1剂量下，C57BL/6J小鼠肝脏DNA损伤(洗脱常数)分别增加2.3倍、2.4倍和4.9倍，而在相同的三个剂量下，DBA/2小鼠分别增加1.9倍、2.1倍和2.3倍。1、2和4 mg endrin kg - 1剂量下，C57BL/6J腹腔巨噬细胞产生的一氧化氮分别增加了1.3倍、1.7倍和2.0倍，而相同剂量下DBA/2小鼠腹腔巨噬细胞产生的一氧化氮分别增加了1.7倍、1.7倍和1.8倍。结果表明，与DBA/2小鼠相比，C57BL/6J小鼠腹膜巨噬细胞对DNA损伤和一氧化氮产生的反应性更具剂量依赖性，而两种小鼠品系的肝线粒体和微粒体脂质过氧化也有类似的结果。结果表明，与二恶英2,3,7,8-四氯二苯并-对二恶英(TCDD)相比，endrin的毒性较少依赖于可能涉及Ah受体系统的机制。
{"title":"Comparative effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide production by peritoneal macrophages from C57BL/6J and DBA/2 mice","authors":"M. Bagchi, E. Hassoun, P. Akubue, D. Bagchi, S.J. Stohs","doi":"10.1016/0742-8413(93)90096-4","DOIUrl":"10.1016/0742-8413(93)90096-4","url":null,"abstract":"<div><p>1. Endrin is a polyhalogenated cyclic hydrocarbon which produces hepatic and neurologic toxicity. In order to further assess the mechanism of toxicity ofendrin, the dose-dependent effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide (NO) production by peritoneal exudate cells (primarily macrophages) were investigated in C57BL/6J and DBA/2 mice which vary at the Ah receptor genetic locus. C57BL/6J mice are dioxin-responsive, while DBA/2 mice are dioxin-insensitive.</p><p>2. Mice of both strains were treated with 0, 1, 2 or 4 mg endrin kg<sup>−1</sup> as a single oral dose in corn oil, and the animals were killed 24 hr post-treatment. At doses of 1,2 and 4 mg endrin kg<sup>−1</sup> in C57BL/6J mice, hepatic mitochondrial lipid peroxidation increased 1.2-, 2.2- and 3.2-fold, respectively, and 1.8-, 2.3- and 3.5-fold with microsomes, respectively. At these same doses in DBA/2 mice, hepatic mitochondrial lipid peroxidation increased 1.3-, 2.0- and 2.6-fold, respectively, and 1.5-, 1.9- and 2.5-fold with microsomes, respectively.</p><p>3. Increases of 2.3-, 2.4- and 4.9-fold were observed in hepatic DNA damage (elution constants) in C57BL/6J mice at doses of 1, 2 and 4 mg endrin kg<sup>−1</sup>, respectively, while at these same three doses, increases of 1.9-, 2.1- and 2.3-fold were observed for DBA/2 mice, respectively.</p><p>4. Nitric oxide production by peritoneal macrophages from C57BL/6J increased by 1.3-, 1.7- and 2.0-fold with doses of 1, 2 and 4 mg endrin kg<sup>−1</sup>, respectively, while in macrophages from DBA/2 mice at these same doses, increases of 1.7-, 1.7- and 1.8-fold, respectively, were observed.</p><p>5. The results indicate that the responsiveness of peritoneal macrophages with respect to both DNA damage and nitric oxide production are more dose-dependent in C57BL/6J mice as compared to DBA/2 mice, while similar results are observed with the lipid peroxidation of hepatic mitochondria and microsomes of the two mouse strains. The results suggest that the toxicity of endrin is less reliant on a mechanism which may involve the Ah receptor system as compared to dioxins as 2,3,7,8-tetrachlorodibenzo-<em>p</em>-dioxin (TCDD).</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 525-529"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90096-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901046","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 : 1993-07-01DOI: 10.1016/0742-8413(93)90071-R
Syed M. Naqvi , Chetana Vaishnavi
1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca2+ and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain).
2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g. crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation.
3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized, (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetyleholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium, (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred, (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume.
4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in the interalveolar partitions of rat's lungs.
5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg2+ ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium.
6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced.
7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3β-hydroxysteroid transferase and 17β-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were notic
{"title":"Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals","authors":"Syed M. Naqvi , Chetana Vaishnavi","doi":"10.1016/0742-8413(93)90071-R","DOIUrl":"10.1016/0742-8413(93)90071-R","url":null,"abstract":"<div><p>1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca<sup>2+</sup> and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain).</p><p>2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g. crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation.</p><p>3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized, (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetyleholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium, (c) Hepatotoxicity: chemically-induced aminopyrine <em>N</em>-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred, (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume.</p><p>4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in the interalveolar partitions of rat's lungs.</p><p>5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na<sup>+</sup>, K<sup>+</sup> and Mg<sup>2+</sup> ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium.</p><p>6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced.</p><p>7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3β-hydroxysteroid transferase and 17β-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were notic","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 347-361"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90071-R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18897671","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 : 1993-07-01DOI: 10.1016/0742-8413(93)90075-V
S.M. Mahmod , H. Huddart
1. Single sucrose gap recordings showed that spontaneous action potentials of rat ileal smooth muscle consisted of slow waves and superimposed spikes which generated rhythmic contractions. As external potassium was raised, the resting potential progressively depolarized.
2. Calcium-free salines inhibited spontaneous mechanical activity and inhibited the plateau phase of the action potential, but spontaneous spike depolarizations persisted.
3. Verapamil, nifedipine and diltiazem all inhibited spontaneous mechanical activity and the plateau phase of the action potential, while in addition diltiazem augmented spike amplitude.
4. Mn ions also inhibited mechanical activity and the action potential plateau, without affecting spike activity while the calcium ionophore A23187 enhanced both mechanical and electrical activity with a pronounced effect on spike amplitude.
5. These results are consistent with the view that the plateau phase of the ileal smooth muscle action potential is dependent upon an influx of extracellular calcium possibly through voltage dependent slow calcium channels.
{"title":"Calcium dependence of electrical and mechanical activity in rat ileum examined by the sucrose-gap technique","authors":"S.M. Mahmod , H. Huddart","doi":"10.1016/0742-8413(93)90075-V","DOIUrl":"10.1016/0742-8413(93)90075-V","url":null,"abstract":"<div><p>1. Single sucrose gap recordings showed that spontaneous action potentials of rat ileal smooth muscle consisted of slow waves and superimposed spikes which generated rhythmic contractions. As external potassium was raised, the resting potential progressively depolarized.</p><p>2. Calcium-free salines inhibited spontaneous mechanical activity and inhibited the plateau phase of the action potential, but spontaneous spike depolarizations persisted.</p><p>3. Verapamil, nifedipine and diltiazem all inhibited spontaneous mechanical activity and the plateau phase of the action potential, while in addition diltiazem augmented spike amplitude.</p><p>4. Mn ions also inhibited mechanical activity and the action potential plateau, without affecting spike activity while the calcium ionophore A23187 enhanced both mechanical and electrical activity with a pronounced effect on spike amplitude.</p><p>5. These results are consistent with the view that the plateau phase of the ileal smooth muscle action potential is dependent upon an influx of extracellular calcium possibly through voltage dependent slow calcium channels.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 387-391"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90075-V","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18897673","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 : 1993-07-01DOI: 10.1016/0742-8413(93)90070-2
E.W. Haeffner
1. Properties, distribution and multiplicity of phosphoinositidases (phospholipase C, PLC) are investigated.
2. Generation of diacylglycerol (DAG) by a variety of enzymes such as phosphoinositide and phosphatidylcholine specific PLC, by a combination of phospholipase D and phosphatidic hydrolase, and by triglyceride lipase is examined.
3. Ca2+ and phospholipid-dependent protein kinase C act as the target of DAG messenger action.
4. There are differences in the formation of DAG in normal and transformal cell.
{"title":"Diacylglycerol: Formation and function in phospholipid-mediated signal transduction","authors":"E.W. Haeffner","doi":"10.1016/0742-8413(93)90070-2","DOIUrl":"10.1016/0742-8413(93)90070-2","url":null,"abstract":"<div><p>1. Properties, distribution and multiplicity of phosphoinositidases (phospholipase C, PLC) are investigated.</p><p>2. Generation of diacylglycerol (DAG) by a variety of enzymes such as phosphoinositide and phosphatidylcholine specific PLC, by a combination of phospholipase D and phosphatidic hydrolase, and by triglyceride lipase is examined.</p><p>3. Ca<sup>2+</sup> and phospholipid-dependent protein kinase C act as the target of DAG messenger action.</p><p>4. There are differences in the formation of DAG in normal and transformal cell.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 337-345"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90070-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18897028","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 : 1993-07-01DOI: 10.1016/0742-8413(93)90074-U
Brenda Oppert, Thomas D. Morgan, Christina Culbertson, Karl J. Kramer
1. Combinations of a cysteine proteinase inhibitor (CPI) and serine proteinase inhibitors (SPI) in wheat germ diets were toxic to larvae of the red flour beetle, Tribolium castaneum, when tested at levels where individual inhibitors were nontoxic.
2. Mixtures of 0.1% (w/w) CPI (E-64) plus 1% of either of three plant SPIs (soybean Kunitz trypsin inhibitor, soybean Bowman-Birk trypsin-chymotrypsin inhibitor, or lima bean trypsin inhibitor) inhibited T. castaneum growth, resulting in 82–97% reduction in larval weight gain 17 days after hatching and 40–60% mortality.
3. Supplemention of diet containing 0.1% E-64 plus 1% soybean Kunitz trypsin inhibitor (STI) with a mixture of amino acids at 7% caused a partial reversal of the growth inhibition, with 91% of the larvae surviving.
4. Diet containing 0.1% E-64 plus either 5 or 10% STI resulted in 100% mortality of the larvae during the first or second instar.
5. Addition of a mixture ofamino acids at 20% to the 0.1% E-64 plus 10% STI diet allowed 89% of the larvae to develop into adults.
6. The synergism between different classes of proteinase inhibitors in the insect's diet that enhances growth inhibition and toxicity demonstrates the potential for an insect pest management strategy involving the coordinated manipulation of two or more types of digestive enzyme inhibitor genes in plants.
{"title":"Dietary mixtures of cysteine and serine proteinase inhibitors exhibit synergistic toxicity toward the red flour beetle, Tribolium castaneum","authors":"Brenda Oppert, Thomas D. Morgan, Christina Culbertson, Karl J. Kramer","doi":"10.1016/0742-8413(93)90074-U","DOIUrl":"10.1016/0742-8413(93)90074-U","url":null,"abstract":"<div><p>1. Combinations of a cysteine proteinase inhibitor (CPI) and serine proteinase inhibitors (SPI) in wheat germ diets were toxic to larvae of the red flour beetle, <em>Tribolium castaneum</em>, when tested at levels where individual inhibitors were nontoxic.</p><p>2. Mixtures of 0.1% (w/w) CPI (E-64) plus 1% of either of three plant SPIs (soybean Kunitz trypsin inhibitor, soybean Bowman-Birk trypsin-chymotrypsin inhibitor, or lima bean trypsin inhibitor) inhibited <em>T. castaneum</em> growth, resulting in 82–97% reduction in larval weight gain 17 days after hatching and 40–60% mortality.</p><p>3. Supplemention of diet containing 0.1% E-64 plus 1% soybean Kunitz trypsin inhibitor (STI) with a mixture of amino acids at 7% caused a partial reversal of the growth inhibition, with 91% of the larvae surviving.</p><p>4. Diet containing 0.1% E-64 plus either 5 or 10% STI resulted in 100% mortality of the larvae during the first or second instar.</p><p>5. Addition of a mixture ofamino acids at 20% to the 0.1% E-64 plus 10% STI diet allowed 89% of the larvae to develop into adults.</p><p>6. The synergism between different classes of proteinase inhibitors in the insect's diet that enhances growth inhibition and toxicity demonstrates the potential for an insect pest management strategy involving the coordinated manipulation of two or more types of digestive enzyme inhibitor genes in plants.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 379-385"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90074-U","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54006307","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}
1. In the present study, we investigated the effect of culture on α1-adrenoceptors that mediate chronotropy and on α1-adrenergic signal transduction in neonatal rat cardiac myocytes.
2. The spontaneous beating rate of neonatal rat myocytes after 3 or 7 days in culture was 37.4 ± 4.2 or 102.0 ± 4.3 beats min−, respectively. The α1-adrenoceptor-mediated chronotropic effect of norepinephrine was positive at day 3 of culture. In contrast to day 3 of culture, the neonatal myocytes exhibited a negative chronotropic response to norepinephrine on day 7 of culture. Both of these effects of norepinephrine were completely abolished by prazosin.
3. The affinity (Kd) and/or density (Bmax) of α1-adrenoceptors labeled with [3H]prazosin in membranes from cultured myocytes were not significantly different between day 3 and day 7 of culture.
4. The expression of Gs, Gi, Gq and Go, α-subunits in membranes from cultured myocytes was found to be significantly increased with the passage of culture time by immunoblot analysis. In contrast, no significant differences in Gβ-subunit expression were observed between day 3 and day 7 of culture.
5. Norepinephrine-stimulated inositol 1,4,5-trisphosphate production by radio-binding protein in neonatal myocytes after 7 days of culture was significantly higher than that of the day 3 counterpart.
6. No significant changes in phospholipid and cholesterol contents in membranes from neonatal myocytes were observed with longer culture times.
7. These results suggest that changes in the responsiveness to α1-adrenergic stimulation from positive to negative chronotropy during culture of cardiac myocytes are mediated, at least in part, by functional alterations in the α1-adrenergic signal transduction systems, including both G-protein expression and inositol 1,4,5-trisphosphate production.
{"title":"Characterization of α1-adrenoceptors which mediate chronotropy in neonatal rat cardiac myocytes","authors":"Hisakazu Kimura , Atsushi Miyamoto , Shin Kawana , Hideyo Ohshika","doi":"10.1016/0742-8413(93)90089-4","DOIUrl":"10.1016/0742-8413(93)90089-4","url":null,"abstract":"<div><p>1. In the present study, we investigated the effect of culture on <em>α</em><sub>1</sub>-adrenoceptors that mediate chronotropy and on <em>α</em><sub>1</sub>-adrenergic signal transduction in neonatal rat cardiac myocytes.</p><p>2. The spontaneous beating rate of neonatal rat myocytes after 3 or 7 days in culture was 37.4 ± 4.2 or 102.0 ± 4.3 beats min<sup>−</sup>, respectively. The <em>α</em><sub>1</sub>-adrenoceptor-mediated chronotropic effect of norepinephrine was positive at day 3 of culture. In contrast to day 3 of culture, the neonatal myocytes exhibited a negative chronotropic response to norepinephrine on day 7 of culture. Both of these effects of norepinephrine were completely abolished by prazosin.</p><p>3. The affinity (<em>K</em><sub>d</sub>) and/or density (<em>B</em><sub>max</sub>) of <em>α</em><sub>1</sub>-adrenoceptors labeled with [<sup>3</sup>H]prazosin in membranes from cultured myocytes were not significantly different between day 3 and day 7 of culture.</p><p>4. The expression of G<sub>s</sub>, G<sub>i</sub>, G<sub>q</sub> and G<sub>o</sub>, α-subunits in membranes from cultured myocytes was found to be significantly increased with the passage of culture time by immunoblot analysis. In contrast, no significant differences in G<sub>β</sub>-subunit expression were observed between day 3 and day 7 of culture.</p><p>5. Norepinephrine-stimulated inositol 1,4,5-trisphosphate production by radio-binding protein in neonatal myocytes after 7 days of culture was significantly higher than that of the day 3 counterpart.</p><p>6. No significant changes in phospholipid and cholesterol contents in membranes from neonatal myocytes were observed with longer culture times.</p><p>7. These results suggest that changes in the responsiveness to <em>α</em><sub>1</sub>-adrenergic stimulation from positive to negative chronotropy during culture of cardiac myocytes are mediated, at least in part, by functional alterations in the <em>α</em><sub>1</sub>-adrenergic signal transduction systems, including both G-protein expression and inositol 1,4,5-trisphosphate production.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 479-485"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90089-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901044","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 : 1993-07-01DOI: 10.1016/0742-8413(93)90095-3
Manasses K. Yunmbam, John F. Roberts
1. Trypanosoma brucei brucei -infected mouse models treated with a new antibiotic, reuterin, showed reduction of the levels of parasitemia and prolonged survival of the mice.
2. Cures of the parasitemia were observed in groups of mice treated with combinations of reuterin and suramin or melarsoprol.
3. Reuterin administered in combination with bleomycin or dl-α-difluoromethylornithine showed temporary remission of the parasitemia in groups of mice.
{"title":"In vivo evaluation of reuterin and its combinations with suramin, melarsoprol, dl-α-difluoromethylornithine and bleomycin in mice infected with Trypanosoma brucei brucei","authors":"Manasses K. Yunmbam, John F. Roberts","doi":"10.1016/0742-8413(93)90095-3","DOIUrl":"10.1016/0742-8413(93)90095-3","url":null,"abstract":"<div><p>1. <em>Trypanosoma brucei brucei</em> -infected mouse models treated with a new antibiotic, reuterin, showed reduction of the levels of parasitemia and prolonged survival of the mice.</p><p>2. Cures of the parasitemia were observed in groups of mice treated with combinations of reuterin and suramin or melarsoprol.</p><p>3. Reuterin administered in combination with bleomycin or <span>dl</span>-α-difluoromethylornithine showed temporary remission of the parasitemia in groups of mice.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 521-524"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90095-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18696041","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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