Sodium Pentaborate Prevents Acetaminophen-Induced Hepatorenal Injury by Suppressing Oxidative Stress, Lipid Peroxidation, Apoptosis, and Inflammatory Cytokines in Rats

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dc.authorid0000-0003-1685-0803
dc.authorid0000-0001-6354-6922
dc.authorid0000-0002-8222-5515
dc.authorid0000-0002-8490-2479
dc.contributor.authorAktaş Şenocak, Esra
dc.contributor.authorUtlu, Necati
dc.contributor.authorKurt, Şeyda
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2023-10-11T05:59:43Z
dc.date.available2023-10-11T05:59:43Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractAcetaminophen (N-acetyl-p-aminophenol, APAP, or paracetamol) is one of the drugs that may be damaging to the kidneys and liver when used in excess. In this context, it is vital to treat these side effects on the liver and kidneys with various antioxidants. Diseases have been treated using herbal and mineral remedies since ancient times. The mineral boron, found in rocks and water, is a crucial ingredient with multiple positive biological effects. The primary objective of this research is to determine whether or not boron has a protective effect against the toxicity generated by APAP in rats. Male Sprague-Dawley rats were pretreated orally with boron-source sodium pentaborate (B50 and B100 mg/kg) for 6 days by gastric gavage in order to counteract the toxicity caused by a single dose of APAP (1g/kg). APAP increased lipid peroxidation as well as serum BUN, creatinine concentrations, and serum activities of AST, ALP, and ALT by consuming GSH in liver and kidney tissues. In addition, the activity of antioxidative enzymes, including SOD, CAT, and GPx, was diminished. Inflammatory indicators such as TNF-?, IL-1?, and IL-33 were elevated in conjunction with APAP toxicity. In kidney and liver tissues, APAP dramatically increased the activity of caspase-3 and triggered apoptosis. Sodium pentaborate therapy on a short-term basis reduced biochemical levels despite these effects of APAP.
dc.identifier.doi10.1007/s12011-023-03755-4
dc.identifier.issn0163-4984
dc.identifier.pmid37393388
dc.identifier.scopusqualityQ1
dc.identifier.urihttps:/dx.doi.org10.1007/s12011-023-03755-4
dc.identifier.urihttps://hdl.handle.net/20.500.12451/11128
dc.identifier.wosWOS:001022098200002
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofBiological Trace Element Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectAcetaminophen
dc.subjectInflammation
dc.subjectLipid Peroxidation
dc.subjectOxidative Stress
dc.subjectSodium Pentaborate
dc.titleSodium Pentaborate Prevents Acetaminophen-Induced Hepatorenal Injury by Suppressing Oxidative Stress, Lipid Peroxidation, Apoptosis, and Inflammatory Cytokines in Rats
dc.typeArticle

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