Toxicology Research最新文献

{"title":"Proteomic analysis of toxic effects of short-term cadmium exposure on goat livers.","authors":"Guangyang Liu, Xiaoyun Shen, Yuanfeng Li","doi":"10.1093/toxres/tfae162","DOIUrl":"https://doi.org/10.1093/toxres/tfae162","url":null,"abstract":"<p><p>Food safety is closely related to environmental pollution. It is worth noting that the long-term accumulation of Cd, a toxic heavy metal, in animals may pose a threat to human health through food chain. Previous studies have found that Cd exposure may cause liver metabolic disorders of black goats, but the mechanism of its impact on liver proteome of goats has not been widely studied. Therefore, in this study, ten male goats (Nubian black goat × native black goat) were exposed to Cd via drinking water containing CdCl2 (20 mg Cd·kg - 1·BW) for 30 days (five male goats per group). Blood physiology and liver antioxidant indices in black goats were determined and differentially expressed proteins (DEPs) in the livers of Cd-exposed goats were profiled by using TMT-labelled proteomics. It was found that plasma Hb and RBC levels as well as PCV values were decreased, liver SOD, GSH-Px, T-AOC and CAT levels were decreased, and MDA level was increased in Cd-treated goats, and 630 DEPs (up 326, down 304) in the livers of Cd-treated goats. Proteomics analysis revealed that Cd exposure affected glutathione metabolism and drug metabolism-cytochrome P450. We identified GP×2, GSTM3, and TBXAS1 as potential protein markers of early Cd toxicity in goats. This study provided theoretical basis for early diagnosis of Cd poisoning in goats.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae162"},"PeriodicalIF":2.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386486","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}

{"title":"Serum glucose/potassium ratio as an indicator of early and delayed outcomes of acute carbon monoxide poisoning.","authors":"Alshaimma Mahmoud Elmansy, Dalia Mustafa Hannora, Heba K Khalifa","doi":"10.1093/toxres/tfae168","DOIUrl":"https://doi.org/10.1093/toxres/tfae168","url":null,"abstract":"<p><strong>Background: </strong>Carbon monoxide (CO) poisoning is a major health problem associated with a high rate of severe morbidity and mortality.</p><p><strong>Aims: </strong>This study aimed to evaluate the validity of the serum glucose/potassium (Glu/K) ratio as a quick predictor of both early and delayed unfavorable outcomes following acute CO poisoning.</p><p><strong>Patients and methods: </strong>This prospective cohort study included 136 patients with acute CO poisoning admitted at Tanta Poison Control Center, Egypt, between January 2023 and June 2024. The serum Glu/K ratio was calculated for all patients. The primary outcome was a prediction of mortality. Secondary outcomes were the prediction of delayed neurological sequelae (DNS) within six months after CO exposure, the need for mechanical ventilation, and the need for hyperbaric oxygen. A receiver operating curve analysis was applied to test the performance of the Glu/K ratio in predicting acute CO poisoning outcomes.</p><p><strong>Results: </strong>The mortality rate was 12.5% of patients with acute CO poisoning. Meanwhile, 14.7% of patients developed DNS. Furthermore, mechanical ventilation was required in 16.9% of patients. An elevated Glu/K ratio was significantly associated with the severity of acute CO poisoning. At a cut-off value of >31.62, the Glu/K ratio demonstrated an AUC of 0.649 for predicting mortality. The Glu/K ratio was employed to predict DNS at a cut-off value of 33.10, with a sensitivity of 60.0%, a specificity of 82.76%, and an AUC of 0.692.</p><p><strong>Conclusions: </strong>Early Glu/K ratio may be an effective, reliable, and convenient laboratory predictor of mortality, DNS, and the need for mechanical ventilation in patients with acute CO poisoning.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae168"},"PeriodicalIF":2.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386488","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}

{"title":"\"Exploring therapeutic potential and toxicological profiles of <i>Cuscuta</i> species: insights from pharmacological studies and an anti-cholinergic toxicity report.\"","authors":"Saurabh Dilip Bhandare","doi":"10.1093/toxres/tfae160","DOIUrl":"10.1093/toxres/tfae160","url":null,"abstract":"<p><p>This study examines the therapeutic potential and toxicological profiles of <i>Cuscuta</i> species based on recent pharmacological investigations: \"a therapeutic potential vs. toxicological risks of <i>Cuscuta</i> species: a pharmacological-toxicology dilemma.\" The study encompasses diverse research areas, including the mitigation of Bisphenol A (BPA)-induced ovarian damage using <i>Cuscuta chinensis</i> flavonoids (CCFs), acute and sub-acute toxicity assessments of <i>Cuscuta chinensis Lam.</i> water extract (CLW), and observations on <i>Cuscuta campestris</i> toxicity in horses. In addition, this scientific study discusses the interplant communication dynamics between soybean and the parasitic dodder (<i>Cuscuta australis</i>) under nutrient deficiency conditions. Key significant findings highlight the efficacy of CCFs in alleviating BPA-induced ovarian damage, the safety profile of CLW within specified doses, and clinical manifestations of <i>C. campestris</i> toxicity in horses. Moreover, insights into interplant communication mechanisms emphasise the significance of protein-mediated interactions in nutrient-deficient environments. The report illustrates the potential toxicity of Dodder in humans, and further research findings into its chemical composition and toxicological profiles reveal great data on its phytotoxicity. Greater awareness and understanding of the risks associated with consuming Dodder and other similar plant species are crucial for preventing plant intoxication and have been a significant major focus of the present toxicology study of <i>Cuscuta</i> species. Hence, by addressing these objectives, the scientific study aims to balance the therapeutic benefits of Cuscuta species with their potential toxicological risks, contributing to a more nuanced understanding of their role in pharmacology and toxicology. This dual focus is crucial for guiding future research and informing safe usage practices.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae160"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379551","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}

{"title":"Impacts of gentamycin toxicity: nephroprotective role of guarana through different signaling pathways.","authors":"Adel Qlayel Alkhedaide","doi":"10.1093/toxres/tfae167","DOIUrl":"10.1093/toxres/tfae167","url":null,"abstract":"<p><p>Gentamicin is a widely used aminoglycosidic antibiotic since its discovery. Like any other medication gentamicin causes unwanted side effects such as hepatotoxicity and nephrotoxicity. This study aims to examine the antioxidant effect of the guarana seed extract in protecting renal tissue. Forty male mice were divided into four groups (group one was control with free access to food and water, group two was treated orally with 300 mg/kg of guarana seed extract daily, group three was injected intraperitoneally with 100 mg/kg of gentamicin daily and the fourth group was co-treated with both 300 mg/kg of guarana seed extract orally and injected intraperitoneally with 100 mg/kg of gentamicin daily) for two weeks. Serum levels of urea, creatinine, AST, ALT, IL-1β and IL-6 have significantly elevated in the gentamicin treated group and those changes were not found in the guarana co-treated group. In gentamicin treated mice, a significant reduction was observed in two antioxidants SOD and GPX accompanied by downregulation of Ho-1 and Nrf2 while, that did not happen in the guarana seed extract co-treated group. Histopathology and immunohistochemistry slides show that the guarana seed extract prevents degenerative and necrotic events in tubular epithelial tissues caused by gentamicin toxicity. In conclusion, current data suggest that gentamicin can damage renal tissues when given at 100 mg/kg/day, however, the guarana seed extract may be capable of preventing that event when cotreated with the gentamicin as a supplement.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae167"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379554","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}

{"title":"Dose-dependent effects of silver nanoparticles on cell death modes in mouse blastocysts induced via endoplasmic reticulum stress and mitochondrial apoptosis.","authors":"Cheng-Kai Lee, Fu-Ting Wang, Chien-Hsun Huang, Wen-Hsiung Chan","doi":"10.1093/toxres/tfae158","DOIUrl":"10.1093/toxres/tfae158","url":null,"abstract":"<p><p>In view of the rapidly expanding medical and commercial applications of silver nanoparticles (AgNPs), their potential health risks and environmental effects are a significant growing concern. Earlier research by our group uncovered the embryotoxic potential of AgNPs, showing detrimental impacts of these nanoparticles on both pre- and post-implantation embryonic development. In the current study, we showed that low (50-100 μM) and high (200-400 μM) dose ranges of AgNPs trigger distinct cell death programs affecting mouse embryo development and further explored the underlying mechanisms. Treatment with low concentrations of AgNPs (50-100 μM) triggered ROS generation, in turn, inducing mitochondria-dependent apoptosis, and ultimately, harmful effects on embryo implantation, post-implantation development, and fetal development. Notably, high concentrations of AgNPs (200-400 μM) evoked more high-level ROS generation and endoplasmic reticulum (ER) stress-mediated necrosis. Interestingly, pre-incubation with Trolox, a strong antioxidant, reduced ROS generation in the group treated with 200-400 μM AgNPs to the level induced by 50-100 μM AgNPs, resulting in switching of the cell death mode from necrosis to apoptosis and a significant improvement in the impairment of embryonic development. Our findings additionally indicate that activation of PAK2 is a crucial step in AgNP-triggered apoptosis and sequent detrimental effects on embryonic development. Based on the collective results, we propose that the levels of ROS generated by AgNP treatment of embryos serve as a critical regulator of cell death type, leading to differential degrees of damage to embryo implantation, post-implantation development and fetal development through triggering apoptosis, necrosis or other cell death signaling cascades.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae158"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379553","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}

{"title":"Di(2-ethylhexyl) phthalate exposure aggravates hypoxia/reoxygenation injury in cerebral endothelial cells by downregulating epithelial cadherin expression.","authors":"Jin Hee Kim, Jae Hoon Lee, Zhengyu Nan, Ja Woo Choi, Jong Wook Song","doi":"10.1093/toxres/tfae163","DOIUrl":"10.1093/toxres/tfae163","url":null,"abstract":"<p><p>Di-(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer that has adverse health effects. Most phthalates exhibit reproductive toxicity and are associated with diseases such as cardiovascular disorders. However, the effect of DEHP exposure on acute hypoxia/reperfusion injury remains unknown. Therefore, we assessed whether hypoxia/reperfusion injury is aggravated by exposure to DEHP and investigated plausible underlying mechanisms, including oxidative stress and expression of cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) and endothelial junctional proteins. bEnd.3 cells were exposed to DEHP and subsequently subjected to oxygen-glucose deprivation (OGD). Cell viability was analyzed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) proliferation assay. The effect of DEHP/OGD/reoxygenation (R) was evaluated by assessing the levels of NO, reactive oxygen species (ROS), and PGE2. The expression of COX-2, cleaved caspase-3, cleaved PARP, inducible nitric oxide synthase (iNOS), and the endothelial tight junction proteins claudin-5 and ZO-1 was evaluated using quantitative polymerase chain reaction and western blotting. OGD/R decreased cell viability, and DEHP exposure before OGD/R further aggravated cell viability. DEHP/OGD/R significantly increased NO, PGE2, and ROS production following OGD/R. In the DEHP/OGD/R group, iNOS, COX-2, cleaved caspase-3, and cleaved PARP expression increased, and claudin-5 and ZO-1 levels decreased compared with those in the OGD/R group. E-Cadherin expression decreased significantly after DEHP/OGD/R exposure compared with that after OGD/R; this decrease in expression was recovered by treatment with the COX-2 inhibitor indomethacin and antioxidant N-acetylcysteine. Exposure to DEHP exacerbated hypoxia-reoxygenation injury. The enhanced damage upon DEHP exposure was associated with increased oxidative stress and COX-2 expression, leading to E-cadherin downregulation and increased apoptosis.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae163"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379552","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}

{"title":"Role of bone marrow mesenchymal stem cell-derived exosomes in reducing neurotoxicity and depression-like behaviors induced by doxorubicin in rats.","authors":"Doaa R I Abdel-Gawad, Fatma Khalil, Olfat Shehata, Marwa A Ibrahim, SalmaI El-Samannoudy, Emad A Mahdi, Nema S Shaban","doi":"10.1093/toxres/tfae159","DOIUrl":"10.1093/toxres/tfae159","url":null,"abstract":"<p><strong>Background: </strong>Doxorubicin (DOX) is a broad-spectrum antitumor drug while its use is limited nowadays due to its neurobiological side effects associated with depression. Bone marrow mesenchymal stem cells (BM-MSCs) derived exosomes are a promising regenerative therapy. In this study, we investigated the therapeutic potentiality of BM-MSCs derived exosomes against the neurotoxicity induced by DOX.</p><p><strong>Methods: </strong>Twenty-four male albino rats were divided equally in to three groups as follow: group 1 (control), group 2 (rats injected intraperitoneally (i.p|) with DOX at a dose 2.5mg/Kg), and group 3 (rats injected with DOX and BM-MSCs derived exosomes i.p at a dose 1.5ml/Kg). During the experiment the behavior tests were noted, after three weeks rats were sacrificed, serum and brain samples were collected for biochemical, molecular and histopathological examinations.</p><p><strong>Results: </strong>The results revealed that DOX causing impairment of the locomotor and increasing the anxiety like behavior of rats, marked neuropathological changes, significant elevation of MDA content and TNF-α concentration, reduction of phospholipase (PLD) and acetylcholinesterase (AChE) protein concentration in addition, there were up regulation of JNK, NF-κB and p38 genes and down regulation of Erk1.</p><p><strong>Conclusion: </strong>Exosomal therapy improved the substantial neurotoxicity of DOX through modulating the markers involved in the neurotoxic signalling pathway of DOX that resulting in improving the pathological lesions and the animal behaviours.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae159"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379555","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}

{"title":"Transcriptomic analysis reveals transcription factors implicated in radon-induced lung carcinogenesis.","authors":"Xing Liu, Yuting Peng, Ruobing Chen, Yueyue Zhou, Xihuan Zou, Mingzhu Xia, Xinyi Wu, Meng Yu","doi":"10.1093/toxres/tfae161","DOIUrl":"10.1093/toxres/tfae161","url":null,"abstract":"<p><strong>Background: </strong>Radon, a potent carcinogen, is a significant catalyst for lung cancer development. However, the molecular mechanisms triggering radon-induced lung cancer remain elusive.</p><p><strong>Methods: </strong>Utilizing a radon exposure concentration of 20,000 Bq/m3 for 20 min/session, malignant transformation was induced in human bronchial epithelial cells (BEAS-2B).</p><p><strong>Results: </strong>Radon-exposed cells derived from passage 25 (BEAS-2B-Rn) exhibited enhanced proliferation and increased colony formation. Analysis of differential gene expression (DEG) through transcription factors revealed 663 up-regulated and 894 down-regulated genes in radon-exposed cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed significant alterations in the malignant transformation pathway of cells, including those related to cancer and the PI3K/AKT signaling pathway. A PPI network analysis indicated a significant association of oncogenes, such as CCND1, KIT, and GATA3, with lung cancer among differentially expressed genes. In addition, the stability of the housekeeping gene was determined through RT-qPCR analysis, which also confirmed the results of transcriptome analysis.</p><p><strong>Conclusions: </strong>The results suggest that transcription factors may play a pivotal role in conferring a survival advantage to radon-exposed cells. This is achieved by malignant transformation of human bronchial epithelial cells into lung carcinogenesis cell phenotypes.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae161"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379556","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}

{"title":"Exploring the potential of selenium nanoparticles and fabricated selenium nanoparticles @vitamin C nanocomposite in mitigating nicotine-induced testicular toxicity in rats.","authors":"Rabab F Hindawy, Rana M M Refaat, Atef E Fouda, Mohamed A El-Shishtawy, Adarsh Kumar, Nagi M El-Shafai, Eman M Faruk, Ola E Nafea","doi":"10.1093/toxres/tfae154","DOIUrl":"10.1093/toxres/tfae154","url":null,"abstract":"<p><strong>Background: </strong>The tobacco epidemic signifies a major public health threat. Nicotine (NIC), a major active constituent in tobacco, impedes male fertility and semen quality. This work is implemented to explore the potential of selenium nanoparticles (SeNPs) and the newly fabricated SeNPs @vitamin C (SeNPs@VITC) nanocomposite in mitigating testicular toxicity induced by NIC.</p><p><strong>Materials and methods: </strong>The six groups of 48 adult Wistar rats were designed as follows: the control group injected intraperitoneally with normal saline, the SeNPs group treated orally with 2 mg/kg of SeNPs, the SeNPs@VITC nanocomposite group treated orally with 2 mg/kg of SeNPs@VITC nanocomposite, the NIC group injected intraperitoneally with 1.25 mL/kg of NIC, the NIC+ SeNPs group received SeNPs plus NIC, and the NIC+ SeNPs@VITC nanocomposite group received SeNPs@VITC nanocomposite plus NIC. Treatments were administered over a 28-day period.</p><p><strong>Results: </strong>NIC treatment significantly caused poor sperm quality, decreased serum testosterone, increased follicle-stimulating hormone (FSH), luteinizing hormone (LH) concentrations, reduced hemoglobin levels, leukocytosis, disrupted testicular oxidant/antioxidant balance, and disorganized testicular structure. The construction of the novel SeNPs@VITC nanocomposite, compared to NIC plus SeNPs alone, demonstrated a more potent ameliorative effect on NIC-induced reproductive toxicity in adult rats. The SeNPs@VITC nanocomposite significantly increased sperm count, reduced the percentage of sperm head abnormalities, lowered both serum FSH and LH concentrations, and improved the hemoglobin response.</p><p><strong>Conclusions: </strong>Both SeNPs and SeNPs@VITC nanocomposite alleviated the testicular toxicity induced by NIC, but the SeNPs@VITC nanocomposite exhibited superior efficacy. The SeNPs@VITC nanocomposite could be employed to advance enhanced therapeutic strategies for addressing male infertility.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae154"},"PeriodicalIF":2.2,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363542","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}

{"title":"Assessment of the toxic influence of locally formulated pesticides on hepatic and renal biomarkers in male Wistar rats.","authors":"Esther Itunuoluwa Adeyele, Esther Olutomilayo Ayanyemi, Rufus Ojo Akomolafe, Olaoluwa Olukiran Sesan, Omolara Titilayo Aladesanmi, Aderonke Okoya Adetutu","doi":"10.1093/toxres/tfae157","DOIUrl":"10.1093/toxres/tfae157","url":null,"abstract":"<p><strong>Background: </strong>There is growing concern of the potential damage to vital organs after long term exposure to locally formulated pesticides in rural area of Nigeria. This study was designed to assessed the effects of the individual chemical compound and their combination on the kidney and liver of rats' model.</p><p><strong>Methodology: </strong>Fifty-four rats divided into six groups and three sub-groups were exposed to 25, 50 and 75% dose of each of the pesticide's LD₅₀ for 4 h at 3 days interval in an inhalation chamber for 28 days. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TOT_BIL), creatinine and urea assay showed significant increase at the aforementioned doses in comparison to the control group. The red blood cell counts, hematocrit and hemoglobin concentrations were significantly altered in the rats administered varying doses of the pesticides when compared with the control. Similar result was obtained for the differential white blood cell counts. Histopathological examinations of the liver tissue of rats showed infiltrated sinusoids, traces of karypyknosis, vacuolar degeneration and microvesicular steatosis while that of the renal tissue showed glomeruli atrophy leading to widened Bowman's spaces as well as few shrunken glomeruli and varied level of degenerative tubular changes to tubular necrosis.</p><p><strong>Conclusion: </strong>This study established that individual pesticides and their mixture is toxic to the liver and kidney, as evidenced by the elevated markers of renal and liver functions and distortion of the structure of both organs as revealed by their photomicrographs. Therefore, it is a matter of public health significance to regularly monitor pesticide residues in foods and humans in order to assess the food safety risk and population exposure to pesticides.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae157"},"PeriodicalIF":2.2,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363541","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}