1. Quercetin ameliorates the hepatic apoptosis of foetal rats induced by in utero exposure to fenitrothion via the transcriptional regulation of paraoxonase-1 and apoptosis-related genes.
- Author
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Ibrahim KA, Eleyan M, Khwanes SA, Mohamed RA, and Abd El-Rahman HA
- Subjects
- Acetylcholinesterase genetics, Acetylcholinesterase metabolism, Animals, Apoptosis drug effects, Aryldialkylphosphatase metabolism, Caspase 9 genetics, Caspase 9 metabolism, Catalase genetics, Catalase metabolism, Chemical and Drug Induced Liver Injury genetics, Chemical and Drug Induced Liver Injury metabolism, Chemical and Drug Induced Liver Injury pathology, Female, Fenitrothion toxicity, Fetus, Gene Expression Regulation, Glutathione Transferase genetics, Glutathione Transferase metabolism, Hepatocytes drug effects, Hepatocytes metabolism, Hepatocytes pathology, Insecticides antagonists & inhibitors, Insecticides toxicity, Liver drug effects, Liver metabolism, Liver pathology, Male, Nitric Oxide metabolism, Oxidative Stress, Pregnancy, Prenatal Exposure Delayed Effects genetics, Prenatal Exposure Delayed Effects metabolism, Prenatal Exposure Delayed Effects pathology, Protein Carbonylation drug effects, Rats, Superoxide Dismutase genetics, Superoxide Dismutase metabolism, Thiobarbituric Acid Reactive Substances metabolism, Tumor Suppressor Protein p53 genetics, Tumor Suppressor Protein p53 metabolism, bcl-2-Associated X Protein genetics, bcl-2-Associated X Protein metabolism, Antioxidants pharmacology, Aryldialkylphosphatase genetics, Chemical and Drug Induced Liver Injury prevention & control, Fenitrothion antagonists & inhibitors, Prenatal Exposure Delayed Effects prevention & control, Quercetin pharmacology
- Abstract
Background & Purpose: Exposure to organophosphorus during different phases of pregnancy induces many adverse impacts on the developing foetuses due to their immature detoxification system. We have estimated the potential amelioration role of quercetin against hepatic injury-induced apoptosis in rat foetuses following gestational exposure to fenitrothion and probable involvement of paraoxonase-1., Methods: Forty pregnant rats were allocated into four groups; the first one kept as control, the second intubated with quercetin (100 mg/kg), the third orally administrated fenitrothion (4.62 mg/kg) and the last group received quercetin two hours before fenitrothion intoxication., Results: Fenitrothion significantly elevated the foetal hepatic levels of thiobarbituric acid reactive substances, protein carbonyl, and nitric oxide, but it reduced the enzymatic activities of glutathione-S-transferase, superoxide dismutase, catalase, and acetylcholinesterase. Furthermore, fenitrothion provoked many histopathological changes in the foetal liver and markedly up-regulated the mRNA gene expression of p53, caspase-9 along with elevation in the immunoreactivity of Bax and caspase-3, but it down-regulated the expression level of paraoxonase-1. Remarkably, quercetin co-treatment successfully ameliorated the hepatic oxidative injury and apoptosis prompted by fenitrothion., Conclusions: Dietary supplements with quercetin can be used to reduce the risk from organophosphorus exposure probably through paraoxonase-1 up-regulation and enhancement of the cellular antioxidant system.
- Published
- 2021
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