Pub Date : 2025-10-01Epub Date: 2024-11-11DOI: 10.1007/s12291-024-01278-w
Ghizal Fatima, Abbas Ali Mahdi, Hekmat B Alhmadi, Oleg Medvedev
Hydrogen sulfide (H2S), once recognized as a harmful gas, is now emerging as a very significant biological substance with great emphasis on neuroprotection and neuromodulation. It has several functions within the nervous system, placing its physiological activities, biochemical characteristics as well as therapeutic possibilities to their proper perspective. Endogenously produced by cystathione beta-synthase (CBS), cystathione gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST) enzymes, H2S is a unique naturally occurring substance that contains multiple biological activities; it is anti-inflammatory, antioxidant, and anti-apoptotic. Such activity allows H2S to reduce oxidative stress, which limits mechanisms of cell death and prevents disruption of mitochondria and thus neuronal injury. H2S can also be regarded as a neuromodulator because it interacts with and affects the glutamatergic, dopaminergic and GABAergic systems at the synaptic level as well as on neurotransmitter systems and synapse dynamics. It modulates synaptic transmission and its plasticity which is essential for cognitive as well as motor activities and exhibits anti-inflammatory effects which are helpful in the progress of the neurodegenerative condition. Recently gathered some evidence emphasizes as well the possible use of H2S in therapeutic interventions in Alzheimer's disease, Parkinson's disease and stroke. In the models of Alzheimer's disease, H2S is able to reduce the toxicity of amyloid-beta peptides and improve cognitive performance. In Parkinson's disease, it protects dopaminergic neurons and reduces the severity of motor deficits. Moreover, H2S provides protection in ischemic stroke models through decrease of reactive oxygen species and inflammation. Clinical practice with H2S-based therapies seems to have certain hurdles even if preclinical results are promising. Aside from stabilizing H2S in a biologically active form, developing a delivery system for H2S appears a challenge as well. This review will attempt to summarize the existing studies on H2S as neuroprotective and neuromodulatory agents, and their avenues of future use and development.
{"title":"Unveiling Hydrogen Sulfide: A New Frontier in Neuroprotection and Neuromodulation.","authors":"Ghizal Fatima, Abbas Ali Mahdi, Hekmat B Alhmadi, Oleg Medvedev","doi":"10.1007/s12291-024-01278-w","DOIUrl":"10.1007/s12291-024-01278-w","url":null,"abstract":"<p><p>Hydrogen sulfide (H<sub>2</sub>S), once recognized as a harmful gas, is now emerging as a very significant biological substance with great emphasis on neuroprotection and neuromodulation. It has several functions within the nervous system, placing its physiological activities, biochemical characteristics as well as therapeutic possibilities to their proper perspective. Endogenously produced by cystathione beta-synthase (CBS), cystathione gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST) enzymes, H<sub>2</sub>S is a unique naturally occurring substance that contains multiple biological activities; it is anti-inflammatory, antioxidant, and anti-apoptotic. Such activity allows H<sub>2</sub>S to reduce oxidative stress, which limits mechanisms of cell death and prevents disruption of mitochondria and thus neuronal injury. H<sub>2</sub>S can also be regarded as a neuromodulator because it interacts with and affects the glutamatergic, dopaminergic and GABAergic systems at the synaptic level as well as on neurotransmitter systems and synapse dynamics. It modulates synaptic transmission and its plasticity which is essential for cognitive as well as motor activities and exhibits anti-inflammatory effects which are helpful in the progress of the neurodegenerative condition. Recently gathered some evidence emphasizes as well the possible use of H<sub>2</sub>S in therapeutic interventions in Alzheimer's disease, Parkinson's disease and stroke. In the models of Alzheimer's disease, H<sub>2</sub>S is able to reduce the toxicity of amyloid-beta peptides and improve cognitive performance. In Parkinson's disease, it protects dopaminergic neurons and reduces the severity of motor deficits. Moreover, H<sub>2</sub>S provides protection in ischemic stroke models through decrease of reactive oxygen species and inflammation. Clinical practice with H<sub>2</sub>S-based therapies seems to have certain hurdles even if preclinical results are promising. Aside from stabilizing H<sub>2</sub>S in a biologically active form, developing a delivery system for H<sub>2</sub>S appears a challenge as well. This review will attempt to summarize the existing studies on H<sub>2</sub>S as neuroprotective and neuromodulatory agents, and their avenues of future use and development.</p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 4","pages":"540-550"},"PeriodicalIF":1.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039973","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 : 2025-10-01Epub Date: 2025-02-18DOI: 10.1007/s12291-025-01310-7
Yasser Fakri Mustafa
Cancer remains one of the most pressing global health concerns, ranking as the second leading cause of death worldwide. Oxidative stress plays a pivotal role in the initiation and progression of cancer, making antioxidants a critical area of research in cancer prevention and treatment. This review aims to provide a comprehensive analysis of fruit-derived antioxidants and their potential therapeutic applications in combating cancer. In particular, it looks at how bioactive compounds like flavonoids, polyphenols, and essential vitamins found in fruits help to neutralize reactive oxygen species, control gene activity, and stop tumors from spreading and growing. The review brings together new studies from the lab, on animals, and with people that show how fruit-derived antioxidants can help fight cancer, how they change important cellular pathways, and how they might work better when combined with other treatments. Furthermore, it discusses challenges related to bioavailability, standardization, and clinical translation, underscoring the need for more robust clinical trials. This review shows how important it is to include antioxidants from fruits in dietary guidelines and move forward with targeted research into their therapeutic use in cancer management. It does this by looking at the current evidence and pointing out research gaps.
{"title":"Role of Fruit-Derived Antioxidants in Fighting Cancer: A Narrative Review.","authors":"Yasser Fakri Mustafa","doi":"10.1007/s12291-025-01310-7","DOIUrl":"10.1007/s12291-025-01310-7","url":null,"abstract":"<p><p>Cancer remains one of the most pressing global health concerns, ranking as the second leading cause of death worldwide. Oxidative stress plays a pivotal role in the initiation and progression of cancer, making antioxidants a critical area of research in cancer prevention and treatment. This review aims to provide a comprehensive analysis of fruit-derived antioxidants and their potential therapeutic applications in combating cancer. In particular, it looks at how bioactive compounds like flavonoids, polyphenols, and essential vitamins found in fruits help to neutralize reactive oxygen species, control gene activity, and stop tumors from spreading and growing. The review brings together new studies from the lab, on animals, and with people that show how fruit-derived antioxidants can help fight cancer, how they change important cellular pathways, and how they might work better when combined with other treatments. Furthermore, it discusses challenges related to bioavailability, standardization, and clinical translation, underscoring the need for more robust clinical trials. This review shows how important it is to include antioxidants from fruits in dietary guidelines and move forward with targeted research into their therapeutic use in cancer management. It does this by looking at the current evidence and pointing out research gaps.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 4","pages":"522-539"},"PeriodicalIF":1.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039979","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 : 2025-07-01Epub Date: 2024-09-11DOI: 10.1007/s12291-024-01264-2
Sonia Tamanna, Taslimul Jannat, Shrabanti Devi, Zimam Mahmud, Mohammad Shakil Mahmood, Mir Fahim Faisal, Akramul Hasan, Md Zakir Hossain Howlader
Research has shown that endothelial dysfunction due to low nitric oxide (NO) bioavailability is one of the primary causes of preeclampsia (PE). Variations in the eNOS gene may be implicated in reducing NO levels. This study examined the relationship between eNOS gene variations and NO and malondialdehyde (MDA) levels in preeclamptic women and their neonates in Bangladesh. This study compared 100 healthy pregnant women (controls) with 82 preeclampsia-diagnosed women and their newborns. PCR-RFLP was used to detect eNOS gene variants, while spectrophotometric methods were used to measure NO and MDA levels in plasma. The maternal eNOS gene variant rs2070744 exhibited a significant relationship with PE risk, particularly under the dominant model and allele frequency scrutiny. Similarly, the neonatal eNOS gene variant rs2070744 exhibited a robust association with PE risk across various genetic models. The case‒control comparison of the genotypic distribution of NO and MDA in the studied subjects revealed that although PE mothers with TT genotypes had significantly lower NO levels than did the controls, the neonates of PE mothers with TT and CC genotypes showed a significant decrease in NO levels compared to their control groups. Moreover, the PE group and their neonates with the TT and CT genotypes had significantly greater MDA levels than did the control group. These findings illuminate the profound influence of eNOS gene variants on preeclampsia onset, suggesting a potential mechanism involving altered NO production via heightened oxidative stress among affected mothers and neonates. Consequently, screening for eNOS variants and estimating NO levels in pregnant women could offer early identification of those predisposed to PE, thus enabling timely interventions.
Supplementary information: The online version contains supplementary material available at 10.1007/s12291-024-01264-2.
{"title":"Exploring the Associations of Maternal and Neonatal <i>eNOS</i> Gene Variant rs2070744 with Nitric Oxide Levels, Oxidative Stress and Adverse Outcomes in Preeclampsia: A Study in the Bangladeshi Population.","authors":"Sonia Tamanna, Taslimul Jannat, Shrabanti Devi, Zimam Mahmud, Mohammad Shakil Mahmood, Mir Fahim Faisal, Akramul Hasan, Md Zakir Hossain Howlader","doi":"10.1007/s12291-024-01264-2","DOIUrl":"https://doi.org/10.1007/s12291-024-01264-2","url":null,"abstract":"<p><p>Research has shown that endothelial dysfunction due to low nitric oxide (NO) bioavailability is one of the primary causes of preeclampsia (PE). Variations in the <i>eNOS</i> gene may be implicated in reducing NO levels. This study examined the relationship between <i>eNOS</i> gene variations and NO and malondialdehyde (MDA) levels in preeclamptic women and their neonates in Bangladesh. This study compared 100 healthy pregnant women (controls) with 82 preeclampsia-diagnosed women and their newborns. PCR-RFLP was used to detect eNOS gene variants, while spectrophotometric methods were used to measure NO and MDA levels in plasma. The maternal <i>eNOS</i> gene variant rs2070744 exhibited a significant relationship with PE risk, particularly under the dominant model and allele frequency scrutiny. Similarly, the neonatal <i>eNOS</i> gene variant rs2070744 exhibited a robust association with PE risk across various genetic models. The case‒control comparison of the genotypic distribution of NO and MDA in the studied subjects revealed that although PE mothers with TT genotypes had significantly lower NO levels than did the controls, the neonates of PE mothers with TT and CC genotypes showed a significant decrease in NO levels compared to their control groups. Moreover, the PE group and their neonates with the TT and CT genotypes had significantly greater MDA levels than did the control group. These findings illuminate the profound influence of <i>eNOS</i> gene variants on preeclampsia onset, suggesting a potential mechanism involving altered NO production via heightened oxidative stress among affected mothers and neonates. Consequently, screening for eNOS variants and estimating NO levels in pregnant women could offer early identification of those predisposed to PE, thus enabling timely interventions.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s12291-024-01264-2.</p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 3","pages":"479-487"},"PeriodicalIF":1.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583795","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 : 2025-07-01Epub Date: 2024-06-19DOI: 10.1007/s12291-024-01200-4
Vandana Rai, Pradeep Kumar
Polycystic ovary syndrome (PCOS) is the most common form of endocrinopathy of women. Several studies have investigated the association of methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism with PCOS risk but the results are contradictory. So, the aim of the present study was to carry out a meta-analysis of a published case control studies to find out exact association between MTHFR gene C677T polymorphism and PCOS susceptibility. Pubmed, Springer link, Science Direct and Google Scholar databases were searched for case-control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) was used as association measure and meta-analysis was performed using MIX and MetaAnalyst programs. Meta-analysis of 24 studies showed strong significant association between C677T polymorphism and PCOS risk (OR: T vs. C = 1.18, 95% CI 1.01-1.38, p = 0.03; OR: TT vs. CC = 1.37, 95% CI 1.0-1.89, p = 0.04; OR: TT + CT vs. CC = 1.31, 95% CI 1.07-1.62, p = 0.008; OR: CT vs. CC = 1.31, 95% CI 1.04-1.62, p = 0.02 and OR: TT vs. CT + CC = 1.10, 95% CI = 0.82-1.47, p = 0.04). In subgroup analysis, MTHFR C677T polymorphism is significantly associated with PCOS risk with Asian individuals but in Caucasian population MTHFR C677T polymorphism was not significantly associated with PCOS risk. In conclusion, C677T polymorphism is a risk factor for PCOS.
多囊卵巢综合征(PCOS)是女性最常见的内分泌疾病。一些研究调查了亚甲基四氢叶酸还原酶(MTHFR)基因C677T多态性与PCOS风险的关系,但结果相互矛盾。因此,本研究的目的是对已发表的病例对照研究进行meta分析,以找出MTHFR基因C677T多态性与PCOS易感性之间的确切关系。检索Pubmed、施普林格link、Science Direct和谷歌Scholar数据库进行病例对照研究。比值比(ORs)和95%置信区间(CIs)作为关联度量,使用MIX和MetaAnalyst程序进行meta分析。24项研究的荟萃分析显示,C677T多态性与PCOS风险之间存在显著相关性(OR: T vs. C = 1.18, 95% CI 1.01-1.38, p = 0.03;OR: TT vs. CC = 1.37, 95% CI 1.0 ~ 1.89, p = 0.04;或:TT + CT与CC = 1.31, 95% CI 1.07 - -1.62, p = 0.008;或者:CT与CC = 1.31, 95% CI 1.04 - -1.62, p = 0.02或:TT和CT + CC = 1.10, 95% CI -1.47 = 0.82, p = 0.04)。在亚组分析中,MTHFR C677T多态性与亚洲个体的PCOS风险显著相关,而在高加索人群中,MTHFR C677T多态性与PCOS风险无显著相关性。综上所述,C677T多态性是PCOS的危险因素。
{"title":"Association Between Methylenetetrahydrofoate Reductase Gene C677T Polymorphism and Susceptibility to Polycystic Ovary Syndrome.","authors":"Vandana Rai, Pradeep Kumar","doi":"10.1007/s12291-024-01200-4","DOIUrl":"https://doi.org/10.1007/s12291-024-01200-4","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is the most common form of endocrinopathy of women. Several studies have investigated the association of methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism with PCOS risk but the results are contradictory. So, the aim of the present study was to carry out a meta-analysis of a published case control studies to find out exact association between MTHFR gene C677T polymorphism and PCOS susceptibility. Pubmed, Springer link, Science Direct and Google Scholar databases were searched for case-control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) was used as association measure and meta-analysis was performed using MIX and MetaAnalyst programs. Meta-analysis of 24 studies showed strong significant association between C677T polymorphism and PCOS risk (OR: T vs. C = 1.18, 95% CI 1.01-1.38, <i>p</i> = 0.03; OR: TT vs. CC = 1.37, 95% CI 1.0-1.89, <i>p</i> = 0.04; OR: TT + CT vs. CC = 1.31, 95% CI 1.07-1.62, <i>p</i> = 0.008; OR: CT vs. CC = 1.31, 95% CI 1.04-1.62, <i>p</i> = 0.02 and OR: TT vs. CT + CC = 1.10, 95% CI = 0.82-1.47, <i>p</i> = 0.04). In subgroup analysis, MTHFR C677T polymorphism is significantly associated with PCOS risk with Asian individuals but in Caucasian population MTHFR C677T polymorphism was not significantly associated with PCOS risk. In conclusion, C677T polymorphism is a risk factor for PCOS.</p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 3","pages":"382-391"},"PeriodicalIF":1.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583793","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 : 2025-07-01Epub Date: 2024-09-11DOI: 10.1007/s12291-024-01266-0
Ahmed Ghdhban Al-Ziaydi
Cell culture techniques are the vital basis for the majority of experimental cancer research. Targeting cancer cells metabolism is one of the key strategies for controlling the growth of cancer cells. D-Mannoheptulose (MH) (as Phytotherapy) a specific inhibitor, belonging to hexokinase category, to inhibit glycolysis pathway and Doxorubicin (DXR) (as Chemotherapy) has cytotoxic activity against cancer cells and anti-cancer effects by inducing apoptosis. Evaluating the effect of D-Mannoheptulose and Doxorubicin on the normal and breast cancer cell line by determining their anti-tumor activities. Cell culture of normal human mammary epithelial cells (HMECs) and MCF-7 cell line were achieved by using Minimum Essential Medium (MEM) and RPMI-1640 Medium. D-Mannoheptulose, and Doxorubicin stock and diluted solutions were prepared by using phosphate buffer saline (PBS), and dimethyl sulphoxide (DMSO) respectively. HMECs and MCF7 cell line were treated with MH, and DXR, cytotoxicity ratio was determined by methyl thiazolyl tetrazolium (MTT). The findings of study indicated a substantial increase in the cytotoxicity and antiproliferative effects of MH and DXR depending on the concentration gradient against breast cancer cell lines and IC50 values, while on the other hand, there was no significant cytotoxic effect on normal cells. Results of the study revealed that MH, DXR, can result in inhibiting the growth of breast cancer cell lines. This behaviour was mainly due to the increase in cytotoxicity through inhibiting the glycolysis pathway thereby resulting in apoptosis. This further lead to the decrease in HK activity and hence pyruvate as well as ATP amount. Overall, DXR and MH treatment display effective cytotoxic effects against the studied breast cancer cell lines.
{"title":"Evaluation of D-Mannoheptulose and Doxorubicin as Potential Therapeutic Agents for Breast Cancer by Targeting Glycolysis and Inducing Apoptosis.","authors":"Ahmed Ghdhban Al-Ziaydi","doi":"10.1007/s12291-024-01266-0","DOIUrl":"https://doi.org/10.1007/s12291-024-01266-0","url":null,"abstract":"<p><p>Cell culture techniques are the vital basis for the majority of experimental cancer research. Targeting cancer cells metabolism is one of the key strategies for controlling the growth of cancer cells. D-Mannoheptulose (MH) (as Phytotherapy) a specific inhibitor, belonging to hexokinase category, to inhibit glycolysis pathway and Doxorubicin (DXR) (as Chemotherapy) has cytotoxic activity against cancer cells and anti-cancer effects by inducing apoptosis. Evaluating the effect of D-Mannoheptulose and Doxorubicin on the normal and breast cancer cell line by determining their anti-tumor activities. Cell culture of normal human mammary epithelial cells (HMECs) and MCF-7 cell line were achieved by using Minimum Essential Medium (MEM) and RPMI-1640 Medium. D-Mannoheptulose, and Doxorubicin stock and diluted solutions were prepared by using phosphate buffer saline (PBS), and dimethyl sulphoxide (DMSO) respectively. HMECs and MCF7 cell line were treated with MH, and DXR, cytotoxicity ratio was determined by methyl thiazolyl tetrazolium (MTT). The findings of study indicated a substantial increase in the cytotoxicity and antiproliferative effects of MH and DXR depending on the concentration gradient against breast cancer cell lines and IC50 values, while on the other hand, there was no significant cytotoxic effect on normal cells. Results of the study revealed that MH, DXR, can result in inhibiting the growth of breast cancer cell lines. This behaviour was mainly due to the increase in cytotoxicity through inhibiting the glycolysis pathway thereby resulting in apoptosis. This further lead to the decrease in HK activity and hence pyruvate as well as ATP amount. Overall, DXR and MH treatment display effective cytotoxic effects against the studied breast cancer cell lines.</p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 3","pages":"412-421"},"PeriodicalIF":1.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583794","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 : 2025-07-01Epub Date: 2025-01-13DOI: 10.1007/s12291-024-01297-7
Yasser Fakri Mustafa, Ayman Faris Faisal, Marwa Mohammed Alshaher, Duha Adnan Hassan
Aging is an inevitable, multifaceted biological process characterized by the progressive decline of physiological functions, ultimately leading to increased susceptibility to chronic diseases and mortality. A combination of genetic, lifestyle, and environmental factors, including dietary habits, exposure to pollutants, and ultraviolet radiation, influence this natural phenomenon. The consequences of aging manifest as various health complications, such as cardiovascular diseases, Type 2 diabetes, neurodegenerative disorders, malignancies, and visible signs like dermal dryness and wrinkles. An imbalance between the body's antioxidant defenses and the production of reactive oxygen and nitrogen species leads to oxidative stress, which is a key part of the aging process. This imbalance induces cellular damage, apoptosis, and tissue dysfunction, accelerating age-related decline. Antioxidants, both endogenous and exogenous, play a pivotal role in mitigating oxidative stress by scavenging harmful free radicals. Micronutrients from food, such as certain vitamins, minerals, and phytochemicals, have gotten a lot of attention as exogenous antioxidants that may slow down or fix age-related problems. This review synthesizes findings from comprehensive literature searches on platforms such as PubMed, Scopus, Web of Science, and Google Scholar, encompassing studies published between 2018 and mid-2024. It looks into the biochemical roles and cell mechanisms that these micronutrients use to fight oxidative stress and support healthy aging. Micronutrients that are high in antioxidants, like vitamins A, C, and E; essential trace minerals, like zinc, copper, and selenium; and phytochemicals, like flavonoids, curcumin, and resveratrol, can help restore the body's oxidative balance. But, even though they seem to have good effects, there isn't enough solid scientific evidence to support the use of these micronutrients as anti-aging agents on their own. This review talks about how eating antioxidant-rich foods every day might be a safer and more long-lasting way to help people live longer and lessen the effects of age-related problems.
Graphical abstract:
衰老是一个不可避免的、多方面的生物学过程,其特征是生理功能的逐渐衰退,最终导致对慢性疾病和死亡率的易感性增加。遗传、生活方式和环境因素的结合,包括饮食习惯、接触污染物和紫外线辐射,都会影响这种自然现象。衰老的后果表现为各种健康并发症,如心血管疾病、2型糖尿病、神经退行性疾病、恶性肿瘤,以及皮肤干燥和皱纹等可见迹象。身体的抗氧化防御与活性氧和氮的产生之间的不平衡导致氧化应激,这是衰老过程的关键部分。这种不平衡导致细胞损伤、细胞凋亡和组织功能障碍,加速与年龄相关的衰退。内源性和外源性抗氧化剂通过清除有害自由基在减轻氧化应激中起关键作用。食物中的微量营养素,如某些维生素、矿物质和植物化学物质,作为外源性抗氧化剂得到了很多关注,它们可以减缓或解决与年龄有关的问题。本综述综合了PubMed、Scopus、Web of Science和b谷歌Scholar等平台上的综合文献搜索结果,涵盖了2018年至2024年中期发表的研究。它研究了这些微量营养素用于对抗氧化应激和支持健康衰老的生化作用和细胞机制。富含抗氧化剂的微量营养素,如维生素A、C和E;必需的微量矿物质,如锌、铜和硒;植物化学物质,如类黄酮、姜黄素和白藜芦醇,可以帮助恢复身体的氧化平衡。但是,即使它们似乎有很好的效果,也没有足够可靠的科学证据来支持这些微量营养素本身作为抗衰老剂的使用。这篇综述讨论了为什么每天吃富含抗氧化剂的食物可能是一种更安全、更持久的方式,可以帮助人们延长寿命,减少与年龄有关的问题的影响。图形化的简介:
{"title":"Food-Derived Micronutrients as Alleviators of Age-Related Dysfunction: A Dive into Their Effects and Cellular Mechanisms.","authors":"Yasser Fakri Mustafa, Ayman Faris Faisal, Marwa Mohammed Alshaher, Duha Adnan Hassan","doi":"10.1007/s12291-024-01297-7","DOIUrl":"https://doi.org/10.1007/s12291-024-01297-7","url":null,"abstract":"<p><p>Aging is an inevitable, multifaceted biological process characterized by the progressive decline of physiological functions, ultimately leading to increased susceptibility to chronic diseases and mortality. A combination of genetic, lifestyle, and environmental factors, including dietary habits, exposure to pollutants, and ultraviolet radiation, influence this natural phenomenon. The consequences of aging manifest as various health complications, such as cardiovascular diseases, Type 2 diabetes, neurodegenerative disorders, malignancies, and visible signs like dermal dryness and wrinkles. An imbalance between the body's antioxidant defenses and the production of reactive oxygen and nitrogen species leads to oxidative stress, which is a key part of the aging process. This imbalance induces cellular damage, apoptosis, and tissue dysfunction, accelerating age-related decline. Antioxidants, both endogenous and exogenous, play a pivotal role in mitigating oxidative stress by scavenging harmful free radicals. Micronutrients from food, such as certain vitamins, minerals, and phytochemicals, have gotten a lot of attention as exogenous antioxidants that may slow down or fix age-related problems. This review synthesizes findings from comprehensive literature searches on platforms such as PubMed, Scopus, Web of Science, and Google Scholar, encompassing studies published between 2018 and mid-2024. It looks into the biochemical roles and cell mechanisms that these micronutrients use to fight oxidative stress and support healthy aging. Micronutrients that are high in antioxidants, like vitamins A, C, and E; essential trace minerals, like zinc, copper, and selenium; and phytochemicals, like flavonoids, curcumin, and resveratrol, can help restore the body's oxidative balance. But, even though they seem to have good effects, there isn't enough solid scientific evidence to support the use of these micronutrients as anti-aging agents on their own. This review talks about how eating antioxidant-rich foods every day might be a safer and more long-lasting way to help people live longer and lessen the effects of age-related problems.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 3","pages":"322-338"},"PeriodicalIF":1.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575391","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 : 2025-07-01Epub Date: 2025-06-18DOI: 10.1007/s12291-025-01328-x
Prasenjit Mitra, Shruti Gupta, Praveen Sharma
{"title":"<b>Laboratory Medicine and Sustainability: A Call To Action</b>.","authors":"Prasenjit Mitra, Shruti Gupta, Praveen Sharma","doi":"10.1007/s12291-025-01328-x","DOIUrl":"https://doi.org/10.1007/s12291-025-01328-x","url":null,"abstract":"","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 3","pages":"319-321"},"PeriodicalIF":1.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583792","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}
Investigating the impact of liposomal Cisplatin on oral cancer cell line seeks to optimize drug delivery efficiency, decrease systemic toxicity, and amplify cytotoxicity specifically against malignant cells. Cisplatin was encapsulated within liposomal nanoparticles through thin-film hydration and extrusion methodologies. The physical and chemical characteristics of the nanoparticles, including zeta potential, size, drug load, and polydispersity index (PDI), were examined to evaluate their properties. The release of the drug was studied in a simulated body fluid environment in vitro. The stability of the nanoparticles was evaluated over a period of 45 days under normal bodily conditions. Ultimately, the liposomal formulations' efficacy was assessed in comparison to free drugs through cell viability assays conducted on the human tongue squamous cell carcinoma cell line CAL 27. The liposomal nanoparticles developed exhibited a favorable size range of 170 nm, a zeta potential of - 30 mV, and a low PDI of under 0.19, demonstrating uniform particle sizes. The encapsulation efficiencies were about % 90, and the drug loading capacities were sufficient. The in vitro release profiles displayed a sustained release pattern over 72 h. The liposomal formulations showed improved stability, with no notable changes in physicochemical properties throughout the study period. Cytotoxicity evaluations revealed that the liposomal Cisplatin formulation exhibited a remarkably higher cytotoxic effect on an oral cancer cell line relative to the unencapsulated drug. This research showcases the promise of liposomal formulations in optimizing the clinical efficacy of oral cancer treatments under superior drug delivery, diminished toxicity, and augmented cytotoxicity.
{"title":"Enhancing Cisplatin Delivery via Liposomal Nanoparticles for Oral Cancer Treatment.","authors":"Parizad Ghanbarikondori, Razieh Bagheri Shahzadeh Aliakbari, Elham Saberian, Andrej Jenča, Adriána Petrášová, Janka Jenčová, Azim Akbarzadeh Khayavi","doi":"10.1007/s12291-024-01239-3","DOIUrl":"10.1007/s12291-024-01239-3","url":null,"abstract":"<p><p>Investigating the impact of liposomal Cisplatin on oral cancer cell line seeks to optimize drug delivery efficiency, decrease systemic toxicity, and amplify cytotoxicity specifically against malignant cells. Cisplatin was encapsulated within liposomal nanoparticles through thin-film hydration and extrusion methodologies. The physical and chemical characteristics of the nanoparticles, including zeta potential, size, drug load, and polydispersity index (PDI), were examined to evaluate their properties. The release of the drug was studied in a simulated body fluid environment in vitro. The stability of the nanoparticles was evaluated over a period of 45 days under normal bodily conditions. Ultimately, the liposomal formulations' efficacy was assessed in comparison to free drugs through cell viability assays conducted on the human tongue squamous cell carcinoma cell line CAL 27. The liposomal nanoparticles developed exhibited a favorable size range of 170 nm, a zeta potential of - 30 mV, and a low PDI of under 0.19, demonstrating uniform particle sizes. The encapsulation efficiencies were about % 90, and the drug loading capacities were sufficient. The in vitro release profiles displayed a sustained release pattern over 72 h. The liposomal formulations showed improved stability, with no notable changes in physicochemical properties throughout the study period. Cytotoxicity evaluations revealed that the liposomal Cisplatin formulation exhibited a remarkably higher cytotoxic effect on an oral cancer cell line relative to the unencapsulated drug. This research showcases the promise of liposomal formulations in optimizing the clinical efficacy of oral cancer treatments under superior drug delivery, diminished toxicity, and augmented cytotoxicity.</p>","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 2","pages":"211-217"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692085","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 : 2025-04-01Epub Date: 2025-03-05DOI: 10.1007/s12291-025-01315-2
Manoj Khokhar, Dharmveer Yadav, Praveen Sharma
{"title":"Transforming Healthcare in the Age of Artificial Intelligence: A New Era of Diagnostic Excellence in Laboratory Medicine.","authors":"Manoj Khokhar, Dharmveer Yadav, Praveen Sharma","doi":"10.1007/s12291-025-01315-2","DOIUrl":"10.1007/s12291-025-01315-2","url":null,"abstract":"","PeriodicalId":13280,"journal":{"name":"Indian Journal of Clinical Biochemistry","volume":"40 2","pages":"163-164"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692045","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}