{"title":"THE ATTENUATION OF MERCURIC CHLORIDE TOXICITY BY FLAVONOIDS IN MALE ALBINO RATS IS INDEPENDENT ON THE NUMBER OF HYDROXYL GROUPS ON B-RINGS","authors":"E. El-Hussieny, Marwa M. Matoug, W. El-Sayed","doi":"10.21608/EJZ.2020.26416.1025","DOIUrl":null,"url":null,"abstract":"General exposure to mercury is conceivable since it has been shown to be exacerbated through contaminated water and food. The present study aimed to evaluate three different flavonoids and selenite against mercuric chloride (HgCl2) toxicity in male Wistar rats. The rats were randomly divided into ten groups (n=7) as follows: a control group, groups orally administered with 5 mg/kg body weight of either sodium selenite or HgCl2, groups orally treated with 50 mg/kg of body weight morin, naringin, or hesperetin, and groups that were orally co-administered with HgCl2 and sodium selenite, morin, naringin, or hesperetin. All treatments continued daily for two weeks. HgCl2 toxicity caused significant elevations in the levels/activities of serum total proteins, globulins, total cholesterol, triacylglycerols, tumor necrosis factor-α, interleukin-6, alanine aminotransferase, and γ-glutamyl transpeptidase, as well as hepatic malondialdehyde and catalase. It also caused significant reductions in the hepatic content of reduced glutathione, as well as hemoglobin content and erythrocytes count. Most of these deleterious effects were ameliorated by the concomitant administration of flavonoids or selenite. There was no structure-activity relationship that could be withdrawn from this study. Naringin with the highest number of hydroxyl groups on B-ring and the highest absolute number of hydroxyl groups in general was, with few exceptions, as efficient as the other flavonoids and selenite as well. Every flavonoid had its own biological signature probably due to its metabolism.","PeriodicalId":11659,"journal":{"name":"Egyptian Journal of Zoology","volume":"12 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Egyptian Journal of Zoology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21608/EJZ.2020.26416.1025","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
General exposure to mercury is conceivable since it has been shown to be exacerbated through contaminated water and food. The present study aimed to evaluate three different flavonoids and selenite against mercuric chloride (HgCl2) toxicity in male Wistar rats. The rats were randomly divided into ten groups (n=7) as follows: a control group, groups orally administered with 5 mg/kg body weight of either sodium selenite or HgCl2, groups orally treated with 50 mg/kg of body weight morin, naringin, or hesperetin, and groups that were orally co-administered with HgCl2 and sodium selenite, morin, naringin, or hesperetin. All treatments continued daily for two weeks. HgCl2 toxicity caused significant elevations in the levels/activities of serum total proteins, globulins, total cholesterol, triacylglycerols, tumor necrosis factor-α, interleukin-6, alanine aminotransferase, and γ-glutamyl transpeptidase, as well as hepatic malondialdehyde and catalase. It also caused significant reductions in the hepatic content of reduced glutathione, as well as hemoglobin content and erythrocytes count. Most of these deleterious effects were ameliorated by the concomitant administration of flavonoids or selenite. There was no structure-activity relationship that could be withdrawn from this study. Naringin with the highest number of hydroxyl groups on B-ring and the highest absolute number of hydroxyl groups in general was, with few exceptions, as efficient as the other flavonoids and selenite as well. Every flavonoid had its own biological signature probably due to its metabolism.