Omotayo B Ilesanmi, Esther F Adeogun, Temitope T Odewale, Bruno Chikere
{"title":"Lead exposure-induced changes in hematology and biomarkers of hepatic injury: protective role of TrévoTM supplement.","authors":"Omotayo B Ilesanmi, Esther F Adeogun, Temitope T Odewale, Bruno Chikere","doi":"10.5620/eaht.2022007","DOIUrl":null,"url":null,"abstract":"<p><p>Lead exposure has been linked to health challenges involving multiple organ failure. More than fifty percent of lead present in the human body is accumulated in the liver causing hepatic injury. A major mechanism of lead toxicity is oxidative stress. TrévoTM is a nutritional supplement with numerous bioactive natural products with detoxifying and antioxidant properties. This study was designed to investigate the hepatoprotective effects of TrévoTM dietary supplements against lead-hepatotoxicity in male Wistar rats. Thirty-five healthy animals were divided into five groups of seven each as follows: Group I=control; II=15 mg/kg of lead acetate (PbA); III= 2 mL/kg of TrévoTM + PbA; IV= 5 mL/kg of TrévoTM + PbA;V=5 mL/kg of TrévoTM . Animals were orally treated with TrévoTM for two days before co-administration with PbA intraperitoneally for 12 consecutive days. Animals were sacrificed 24 h after the last administration and blood were collected via cardiac puncture and processed for hematological parameters and assessment of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB). The liver was excised and processed for markers of oxidative stress and histopathological examination. Intraperitoneal administration of 15 mg/kg of PbA caused a significant increase in serum concentration of AST, ALT, while the concentration of ALB was significantly decreased (Plt;0.001). PbA caused a significant reduction in packed cell volume, hemoglobin while the total white blood cell count, neutrophils, lymphocytes, monocytes, eosinophils, and basophils were increased. Oxidative stress was significantly pronounced in the liver of rats exposed to PbA as observed in the high concentration of malonedialdehyde, decreased concentration of glutathione, the activity of catalase, superoxide dismutase, and glutathione-S-transferase. Pretreatment with TrévoTM was able to significantly prevent the anemic, oxidative damage, and hepatic injury initiated by PbA. Histological examination also corroborated the biochemical results. In conclusion, the study reveals that TrévoTM is effective in attenuating PbA-induced hepatotoxicity in male Wistar rats.</p>","PeriodicalId":11867,"journal":{"name":"Environmental analysis, health and toxicology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/06/f1/eaht-37-2-e2022007.PMC9314204.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental analysis, health and toxicology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5620/eaht.2022007","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/4/11 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Lead exposure has been linked to health challenges involving multiple organ failure. More than fifty percent of lead present in the human body is accumulated in the liver causing hepatic injury. A major mechanism of lead toxicity is oxidative stress. TrévoTM is a nutritional supplement with numerous bioactive natural products with detoxifying and antioxidant properties. This study was designed to investigate the hepatoprotective effects of TrévoTM dietary supplements against lead-hepatotoxicity in male Wistar rats. Thirty-five healthy animals were divided into five groups of seven each as follows: Group I=control; II=15 mg/kg of lead acetate (PbA); III= 2 mL/kg of TrévoTM + PbA; IV= 5 mL/kg of TrévoTM + PbA;V=5 mL/kg of TrévoTM . Animals were orally treated with TrévoTM for two days before co-administration with PbA intraperitoneally for 12 consecutive days. Animals were sacrificed 24 h after the last administration and blood were collected via cardiac puncture and processed for hematological parameters and assessment of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB). The liver was excised and processed for markers of oxidative stress and histopathological examination. Intraperitoneal administration of 15 mg/kg of PbA caused a significant increase in serum concentration of AST, ALT, while the concentration of ALB was significantly decreased (Plt;0.001). PbA caused a significant reduction in packed cell volume, hemoglobin while the total white blood cell count, neutrophils, lymphocytes, monocytes, eosinophils, and basophils were increased. Oxidative stress was significantly pronounced in the liver of rats exposed to PbA as observed in the high concentration of malonedialdehyde, decreased concentration of glutathione, the activity of catalase, superoxide dismutase, and glutathione-S-transferase. Pretreatment with TrévoTM was able to significantly prevent the anemic, oxidative damage, and hepatic injury initiated by PbA. Histological examination also corroborated the biochemical results. In conclusion, the study reveals that TrévoTM is effective in attenuating PbA-induced hepatotoxicity in male Wistar rats.