Toxicology Research最新文献_第10页

Network analysis of toxic endpoints of fungicides in zebrafish. 斑马鱼中杀菌剂毒性终点的网络分析。

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-06-05 eCollection Date: 2024-06-01 DOI: 10.1093/toxres/tfae087

Rajesh Pamanji, Prathiviraj Ragothaman, Srikanth Koigoora, Gisha Sivan, Joseph Selvin

{"title":"Network analysis of toxic endpoints of fungicides in zebrafish.","authors":"Rajesh Pamanji, Prathiviraj Ragothaman, Srikanth Koigoora, Gisha Sivan, Joseph Selvin","doi":"10.1093/toxres/tfae087","DOIUrl":"10.1093/toxres/tfae087","url":null,"abstract":"Zebrafish being the best animal model to study, every attempt has been made to decipher the toxic mechanism of every fungicide of usage and interest. It is important to understand the multiple targets of a toxicant to estimate the toxic potential in its totality. A total of 22 fungicides of different classes like amisulbrom, azoxystrobin, carbendazim, carboxin, chlorothalonil, difenoconazole, etridiazole, flusilazole, fluxapyroxad, hexaconazole, kresoxim methyl, mancozeb, myclobutanil, prochloraz, propiconazole, propineb, pyraclostrobin, tebuconazole, thiophanate-methyl, thiram, trifloxystrobin and ziram were reviewed and analyzed for their multiple explored targets in zebrafish. Toxic end points in zebrafish are highly informative when it comes to network analysis. They provide a window into the molecular and cellular pathways that are affected by a certain toxin. This can then be used to gain insights into the underlying mechanisms of toxicity and to draw conclusions on the potential of a particular compound to induce toxicity. This knowledge can then be used to inform decisions about drug development, environmental regulation, and other areas of research. In addition, the use of zebrafish toxic end points can also be used to better understand the effects of environmental pollutants on ecosystems. By understanding the pathways affected by a given toxin, researchers can determine how pollutants may interact with the environment and how this could lead to health or environmental impacts.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 3","pages":"tfae087"},"PeriodicalIF":2.1,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11150978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141285822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Curcumin protects against cadmium-induced germ cell death in the testis of rats. 姜黄素能防止镉诱导的大鼠睾丸生殖细胞死亡。

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-06-04 eCollection Date: 2024-04-01 DOI: 10.1093/toxres/tfae082

Yamin Li, Lu Yang, Ping Su, Na Chen

{"title":"Curcumin protects against cadmium-induced germ cell death in the testis of rats.","authors":"Yamin Li, Lu Yang, Ping Su, Na Chen","doi":"10.1093/toxres/tfae082","DOIUrl":"10.1093/toxres/tfae082","url":null,"abstract":"Introduction: Cadmium (Cd) has been shown to disrupt the reproductive system. In this study, we evaluated the protective effects of Curcumin (Cur) against Cd-induced reproductive toxicity.Methods: Exploring the role of Cur in Cd-treated rat models.Results: The study demonstrated that Cd treatment impaired the seminiferous epithelium, leading to increased apoptosis of germ cells. Interestingly, pretreatment with Cur ameliorated the histological damage and decreased the germ cell apoptosis induced by Cd. Furthermore, after Cd exposure, B-cell lymphoma-2 expression was significantly decreased while Bax expression was increased. Pretreatment of rats with Cur protected against germ cell apoptosis by improving the expression of B-cell lymphoma-2 and reducing Bax. Additionally, Cd treatment increased reactive oxygen species, resulting in a decrease in antioxidant enzymes. However, pretreatment of rats with Cur followed by Cd administration led to a substantial decrease in reactive oxygen species levels and increased activities of antioxidant enzymes. Ultrastructural investigations revealed that damage to the mitochondrial structure was significantly ameliorated by Cur pretreatment in Cd-treated rats. Notably, Cur significantly activated the peroxisome proliferator-activated receptor gamma coactivator 1a/Sirtuins-3 signaling pathway.Conclusions: Overall, our data suggest that Cd induces germ cell apoptosis through mitochondrial-induced oxidative stress, but Cur pretreatment offers strong protection against Cd-induced reproductive toxicity.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 2","pages":"tfae082"},"PeriodicalIF":2.1,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11149375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identifying toxic effects and metabolic perturbations of Duttaphrynus melanostictus skin extracts in human erythrocytes. 确定 Duttaphrynus melanostictus 皮肤提取物对人类红细胞的毒性作用和代谢扰动。

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-06-03 eCollection Date: 2024-06-01 DOI: 10.1093/toxres/tfae086

Fatima F Bebal, Akshay D Bagwe, Roshan C D'Souza, Bharatbhushan B Sharma

{"title":"Identifying toxic effects and metabolic perturbations of Duttaphrynus melanostictus skin extracts in human erythrocytes.","authors":"Fatima F Bebal, Akshay D Bagwe, Roshan C D'Souza, Bharatbhushan B Sharma","doi":"10.1093/toxres/tfae086","DOIUrl":"10.1093/toxres/tfae086","url":null,"abstract":"Background: Skin secretions of toads are widely used in medicine all over the world for their antiviral, anti-infective, and cardiotonic properties. Because these secretions are mostly employed to combat blood parasite infection, it is important to understand their potential toxic effects on human erythrocytes. Therefore, the objective of the current investigation was to elucidate the effects of Duttaphrynus melanostictus (Schneider) skin extracts on the physiology of human erythrocytes.Methods: Toads captured from their natural habitat were separated into three groups according to their body size. Hydroalcoholic extracts of toad skin were prepared by reflux heating. These extracts were then evaluated for their hemolytic and hemoglobin denaturation potential. The effects of the extracts on cytosolic and membrane-bound enzymes of human erythrocytes were assessed.Results: The hemolysis and hemoglobin denaturation caused by these extracts correlated positively with the respective toad sizes. Extracts from medium and large toads led to increased osmotic fragility even at near iso-osmotic concentrations. Biochemical analysis of hemolysate showed that the treatment induced a shift of metabolic flux toward the glutathione pathway. Analysis of membrane-bound enzymes revealed a significant decrease in the activity of Na+/K+ ATPase and acetylcholinesterase. SDS-PAGE analysis of the erythrocyte membrane did not show the band of tropomodulin for the cells treated with 1000 𝜇g/ml extract from large toads.Conclusions: In conclusion, the present study demonstrates that the toxicity of toad skin secretions aggravates with the size of the animal and interferes with the physiology of human erythrocytes, leading to their membrane disruption and rapid lysis.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 3","pages":"tfae086"},"PeriodicalIF":2.1,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11145735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141246754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reproductive toxicity perspectives of nanoparticles: an update. 纳米颗粒的生殖毒性展望：最新进展。

IF 2.2 4区医学

Toxicology Research Pub Date : 2024-05-31 eCollection Date: 2024-06-01 DOI: 10.1093/toxres/tfae077

B Kavya Sree, Nitesh Kumar, Sanjiv Singh

引用次数: 0

STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress. STAT3 诱导的 lncRNA TTN-AS1 上调通过促进氧化应激加重了糖尿病肾病的荚膜细胞损伤。

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-05-31 eCollection Date: 2024-06-01 DOI: 10.1093/toxres/tfae079

Wenzhe Wang, Yongxia Li, Fan Zhu, Yunfang Huang

{"title":"STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress.","authors":"Wenzhe Wang, Yongxia Li, Fan Zhu, Yunfang Huang","doi":"10.1093/toxres/tfae079","DOIUrl":"10.1093/toxres/tfae079","url":null,"abstract":"Background: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus (DM), being the second cause of end-stage renal disease globally. Podocyte injury is closely associated with DN developmen. Our study aimed to investigate the role of long non-coding RNA (lncRNA) TTN-AS1 in DN-associated podocyte injury.Methods: The mouse podocyte cell line (MPC5) and human primary podocytes were stimulated by high glucose (HG; 30 nM glucose) to establish the cellular model of DN. Before HG stimulation, both podocytes were transfected with sh-TTN-AS1#1/2 or pcDNA3.1/STAT3 to evaluate the influence of TTN-AS1 knockdown or STAT3 overexpression on HG-induced podocyte injury. TTN-AS1 and STAT3 expression in both podocytes was examined by RT-qPCR. Cell viability and death were assessed by CCK-8 and LDH release assay. ELISA was adopted for testing IL-6 and TNF-α contents in cell supernatants. The levels of oxidative stress markers (ROS, MDA, SOD, and GSH) in cell supernatants were determined by commercial kits. Western blotting was used for measuring the expression of fibrosis markers (fibronectin and α-SMA and podocyte function markers (podocin and nephrin) in podocytes.Results: HG stimulation led to decreased cell viability, increased cell death, fibrosis, inflammation, cell dysfunction and oxidative stress in podocytes. However, knockdown of TTN-AS1 ameliorated HG-induced podocyte injury. Mechanically, the transcription factor STAT3 interacted with TTN-AS1 promoter and upregulated TTN-AS1 expression. STAT3 overexpression offset the protective effect of TTN-AS1 silencing on HG-induced podocyte damage.Conclusion: Overall, STAT3-mediated upregulation of lncRNA TTN-AS1 could exacerbate podocyte injury in DN through suppressing inflammation and oxidative stress.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 3","pages":"tfae079"},"PeriodicalIF":2.1,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11142850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antioxidant, anti-inflammatory, and anti-DNA damage effects of carnosic acid against aflatoxin B1-induced hepatic, renal, and cardiac toxicities in rats. 肉毒碱对黄曲霉毒素 B1 诱导的大鼠肝、肾和心脏毒性的抗氧化、抗炎和抗 DNA 损伤作用。

IF 2.2 4区医学

Toxicology Research Pub Date : 2024-05-31 eCollection Date: 2024-06-01 DOI: 10.1093/toxres/tfae083

Ghadeer M Albadrani, Ahmed E Altyar, Osama A Kensara, Mohie A M Haridy, Mohamed Sayed Zaazouee, Alaa Ahmed Elshanbary, Amany A Sayed, Mohamed M Abdel-Daim

{"title":"Antioxidant, anti-inflammatory, and anti-DNA damage effects of carnosic acid against aflatoxin B1-induced hepatic, renal, and cardiac toxicities in rats.","authors":"Ghadeer M Albadrani, Ahmed E Altyar, Osama A Kensara, Mohie A M Haridy, Mohamed Sayed Zaazouee, Alaa Ahmed Elshanbary, Amany A Sayed, Mohamed M Abdel-Daim","doi":"10.1093/toxres/tfae083","DOIUrl":"https://doi.org/10.1093/toxres/tfae083","url":null,"abstract":"Background: Aflatoxin B1 (AFB1) food contamination is a global health hazard that has detrimental effects on both human and animal health. The objective of the current study is to assess the protective impact of carnosic acid against AFB1-induced toxicities in the liver, kidneys, and heart.Methods: Forty male Wistar Albino rats (weighting 180 ~ 200 g) were allocated into 5 groups (8 rats each); the 1st group received saline as served as a control, the 2nd group received carnosic acid (CA100) at a dose of 100 mg/kg bw/day by gavage for 14 days, the 3rd group received AFB1 at a dose of 2.5 mg/kg bw, orally twice on days 12 and 14, the 4th group (AFB1-CA50) received AFB1 as in the 3rd group and CA at a dose of 50 mg/kg bw/day, and the 5th group (AFB1-CA100) received AFB1 as in the 3rd group and CA as in the 2nd group.Results: CA significantly decreased the liver enzymes (ALT, AST. ALP), renal function products (LDH, BUN, creatinine), and cardiac enzymes (CK and CK-MB) to control levels after the high increment by AFB1 exposure. Moreover, CA significantly decreased the oxidative stress (MDA, NO, 8-OHdG) and increased the antioxidant enzyme activities (CAT, GSH, GSH-Px, and SOD) after severe disruption of oxidant/antioxidant balance by AFB1 exposure. Interestingly, CA significantly decreased the proinflammatory mediators (IL-6, IL-1β, and TNF-α) to the control levels after severe inflammation induced by AFB1 exposure.Conclusions: Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 3","pages":"tfae083"},"PeriodicalIF":2.2,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11200098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141464493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Therapeutic effects of vitamin B17 against anabolic steroid Trenorol induced testicular toxicity, injury, DNA damage and apoptosis in male rats. 维生素 B17 对同化类固醇特仑诺诱导的雄性大鼠睾丸毒性、损伤、DNA 损伤和凋亡的治疗作用

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-05-29 eCollection Date: 2024-04-01 DOI: 10.1093/toxres/tfae084

Aljohara M Al-Otaibi

{"title":"Therapeutic effects of vitamin B17 against anabolic steroid Trenorol induced testicular toxicity, injury, DNA damage and apoptosis in male rats.","authors":"Aljohara M Al-Otaibi","doi":"10.1093/toxres/tfae084","DOIUrl":"10.1093/toxres/tfae084","url":null,"abstract":"Several anabolic androgenic steroids (ASSs) are a group of synthetic molecules derived from testosterone and developed mainly for veterinary use that classed as a Schedule III and sometimes utilized by athletes to enlarge their muscles. Abuse of anabolic androgenic steroids can result in severe organ damage that cannot be repaired. Therefore; the objective of the current investigation was to examine the therapeutic effects of vitamin B17 (VitB17) on the testicular toxicity caused by the anabolic steroid Trenorol in male rats. Rats were randomly assigned into control, VitB17 (50 mg/kg b.wt./day, orally), Trenorol (received 10 mg/kg b.wt./week, IM) and Trenorol + VitB17 treated groups. At the end of experiment, hormonal assay, semen evaluation, testicular enzymes, and DNA damage were assessed. Besides, the histopathological and immunohistochemical investigations of the P53 expression were performed. Current results revealed that; Trenorol induced significant depletion in relative weights of testis (RWT), total testosterone follicle stimulating hormone (FSH), and luteinizing hormone (LH), sperm count, morphology index, viability, progressive motility, and testicular injury and a significant increase sperm abnormalities, testicular DNA damage and P53 experssions. Treatment of rats with Trenorol + VitB17 decreased the testicular toxicity, sperm parameters, DNA damage and apoptosis. We can conclude that; Trenorol induced toxicity, DNA damage and apoptosis in rat testis and treatments with VitB1 improved these parameters.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 2","pages":"tfae084"},"PeriodicalIF":2.1,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11137343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-osteoporosis activity of casticin in ovariectomized rats. 卵巢切除大鼠体内的可可碱抗骨质疏松症活性

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-04-26 eCollection Date: 2024-04-01 DOI: 10.1093/toxres/tfae064

Dong Zhang, Jianmin Li, Xuejia Li, Wanxin Liu, Ying Yu, Hao Sun, Jiajun Wu, Zhichao Ge, Kai Lv, Yanting Shao, Shuqiang Wang, Xiaojian Ye

{"title":"Anti-osteoporosis activity of casticin in ovariectomized rats.","authors":"Dong Zhang, Jianmin Li, Xuejia Li, Wanxin Liu, Ying Yu, Hao Sun, Jiajun Wu, Zhichao Ge, Kai Lv, Yanting Shao, Shuqiang Wang, Xiaojian Ye","doi":"10.1093/toxres/tfae064","DOIUrl":"https://doi.org/10.1093/toxres/tfae064","url":null,"abstract":"Background: Postmenopausal osteoporosis (PMPO) is the most familiar type of osteoporosis, a silent bone disease. Casticin, a natural flavonoid constituent, improves osteoporosis in animal model. Nevertheless, the potential mechanism remains to be further explored.Methods: A model of PMPO was established in rats treated with ovariectomy (OVX) and RAW 264.7 cells induced with receptor activator of nuclear factor kappa-B ligand (RANKL). The effect and potential mechanism of casticin on PMPO were addressed by pathological staining, measurement of bone mineral density (BMD), three-point bending test, serum biochemical detection, filamentous-actin (F-actin) ring staining, TRAcP staining, reverse transcription quantitative polymerase chain reaction, western blot and examination of oxidative stress indicators.Results: The casticin treatment increased the femoral trabecular area, bone maturity, BMD, elastic modulus, maximum load, the level of calcium and estrogen with the reduced concentrations of alkaline phosphatase (ALP) and tumor necrosis factor (TNF)-α in OVX rats. An enhancement in the F-actin ring formation, TRAcP staining and the relative mRNA expression of NFATc1 and TRAP was observed in RANKL-induced RAW 264.7 cells, which was declined by the treatment of casticin. Moreover, the casticin treatment reversed the reduced the relative protein expression of Nrf2 and HO-1 and the concentrations of superoxide dismutase and glutathione peroxidase, and the increased content of malondialdehyde both in vivo and in vitro.Conclusion: Casticin improved bone density, bone biomechanics, the level of calcium and estrogen, the release of pro-inflammatory factor and oxidative stress to alleviate osteoporosis, which was associated with the upregulation of Nrf2/HO-1 pathway.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 2","pages":"tfae064"},"PeriodicalIF":2.1,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11052697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140846403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ameliorative impacts of sinapic acid against mercuric chloride-induced renal toxicity: role of antioxidants and inflammatory cytokines. 西那皮酸对氯化汞诱发的肾毒性的改善作用：抗氧化剂和炎症细胞因子的作用

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-04-23 eCollection Date: 2024-04-01 DOI: 10.1093/toxres/tfae066

Arshad Mehmood, Mohamed Mohamed Soliman, Daklallah A Almalki, Khalid S Alotaibi, Gehan Basiony Ahmed Youssef, Saed Althobaiti

{"title":"Ameliorative impacts of sinapic acid against mercuric chloride-induced renal toxicity: role of antioxidants and inflammatory cytokines.","authors":"Arshad Mehmood, Mohamed Mohamed Soliman, Daklallah A Almalki, Khalid S Alotaibi, Gehan Basiony Ahmed Youssef, Saed Althobaiti","doi":"10.1093/toxres/tfae066","DOIUrl":"https://doi.org/10.1093/toxres/tfae066","url":null,"abstract":"Because of their beneficial properties, natural products, especially medicinal plants, are becoming increasingly popular worldwide and play a significant role in research. This study was aimed to evaluate the nephroprotective effect of sinapic acid against mercuric chloride-induced renal toxicity in mice. The mice were allocated to four groups named a normal group (G1), model group (G2; received HgCl2, 1 mg/kg bw), treatments groups (G3 and G4: received 50 and 100 mg/kg bw of sinapic acid together with HgCl2). Mice received HgCl2 remarkably showed alteration in all examined biochemical biomarkers (urea, creatinine, and bilirubin), and induced alteration in blood cell picture and anemia. HgCl2 intoxication decreased both systemic and renal antioxidant activity and induced over all oxidative stress as indicated by alteration in inflammation and oxidative stress associated markers. HgCl2 affected renal histology with leukocytic and inflammatory cell infiltration, fibrosis and tubular necrosis. Administration of sinapic acid (50 and 100 mg/kg bw) markedly restored the HgCl2-induced oxidative stress (serum and renal: MDA, GSH, CAT, SOD, and T-AOC), proinflammatory cytokines (serum and renal: TNF-α, IL-6, IL-1β, and PGE2) and restored the changes on biochemical markers, and hematological parameters (hemoglobin, erythrocytes, platelets, and leukocytes). Taken together, the results of the present study disclose that sinapic acid has the potential to attenuate HgCl2-induced renal toxicity and may be an ideal choice against mercury poisoning.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 2","pages":"tfae066"},"PeriodicalIF":2.1,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11036892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140846506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Modulatory potential of Bacopa monnieri against aflatoxin B1 induced biochemical, molecular and histological alterations in rats. 百草枯对黄曲霉毒素 B1 诱导的大鼠生化、分子和组织学改变的调节潜力。

IF 2.1 4区医学

Toxicology Research Pub Date : 2024-04-21 eCollection Date: 2024-04-01 DOI: 10.1093/toxres/tfae060

Arti Rathour, Shamli S Gupte, Divya Gupta, Shubham Singh, Sadhana Shrivastava, Deepa Yadav, Sangeeta Shukla

{"title":"Modulatory potential of Bacopa monnieri against aflatoxin B1 induced biochemical, molecular and histological alterations in rats.","authors":"Arti Rathour, Shamli S Gupte, Divya Gupta, Shubham Singh, Sadhana Shrivastava, Deepa Yadav, Sangeeta Shukla","doi":"10.1093/toxres/tfae060","DOIUrl":"https://doi.org/10.1093/toxres/tfae060","url":null,"abstract":"Oxidative injury is concerned with the pathogenesis of several liver injuries, including those from acute liver failure to cirrhosis. This study was designed to explore the antioxidant activity of Bacopa monnieri (BM) on Aflatoxin B1 (AFB1) induced oxidative damage in Wistar albino rats. Aflatoxin B1 treatment (200 μg/kg/day, p.o.) for 28 days induced oxidative injury by a significant alteration in serum liver function test marker enzymes (AST, ALT, ALP, LDH, albumin and bilirubin), inflammatory cytokines (IL-6, IL-10 and TNF-α), thiobarbituric acid reactive substances (TBARS) along with reduction of antioxidant enzymes (GSH, SOD, CAT), GSH cycle enzymes and drug-metabolizing enzymes (AH and AND). Treatment of rats with B. monnieri (20, 30 and 40 mg/kg for 5 days, p.o.) after 28 days of AFB1 intoxication significantly restored these parameters near control in a dose-dependent way. Histopathological examination disclosed extensive hepatic injuries, characterized by cellular necrosis, infiltration, congestion and sinusoidal dilatation in the AFB1-treated group. Treatment with B. monnieri significantly reduced these toxic effects resulting from AFB1. B. monnieriper se group (40 mg/kg) did not show any significant change and proved safe. The cytotoxic activity of B. monnieri was also evaluated on HepG2 cells and showed a good percentage of cytotoxic activity. This finding suggests that B. monnieri protects the liver against oxidative damage caused by AFB1, which aids in the evaluation of the traditional usage of this medicinal plant.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 2","pages":"tfae060"},"PeriodicalIF":2.1,"publicationDate":"2024-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11033570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140846371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0