Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
Echinochrome guarding effect against sodium arsenite-induced hepatorenal toxicity in rats.
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Sakr Hader I, Atia Tarek, Mahmoud Neamat A, Abdelmawgood Islam Ahmed, Khalaf Marina Lotfy, Ebeed Bassam Waleed, Abdelmohsen Ahmed Mohamed, Kotb Mohamed A, Al Shawoush Abdeljalil Mohamed, Damanhory Ahmed A, Elagali Abdallah Mohammed, Mohamed Ayman Saber, Abdelfattah Hadeer Hesham
Аннотация
BACKGROUND: The persistent and accumulative qualities of the poisonous metalloid arsenic make it a ubiquitous environmental threat. Echinochrome (Ech) is a natural product that possesses antioxidative, antiviral, antialgal, anti-allergic, and antibacterial effects.
AIM: The work investigates the beneficial impact of Ech on sodium arsenite-induced hepatorenal toxicity in rats. Eighteen male rats dispersed equally among three groups: control, sodium arsenite (AS), and AS + Ech. Rats were administered AS (10 mg/kg) and Ech (1 mg/kg BW) by gavage for the experimental duration of 30 days. Ech inhibits oxidative stress by improving antioxidant levels, including glutathione, catalase, and glutathione-S-transferase, with a concomitant decrease in the amounts of malondialdehyde and nitric oxide in kidney and liver tissues. Moreover, it reduced blood concentrations of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, serum urea, uric acid, and creatinine. Concurrently, Ech resulted in a substantial increase in albumin and total protein levels. Additionally, Ech inhibits inflammation by reducing serum concentrations of tumor necrosis factor-α, cyclooxygenase 2, and prostaglandin E2.
CONCLUSION: Ech mitigates arsenic-induced hepatorenal damage by inhibiting oxidative stress and inflammatory pathways.
AIM: The work investigates the beneficial impact of Ech on sodium arsenite-induced hepatorenal toxicity in rats. Eighteen male rats dispersed equally among three groups: control, sodium arsenite (AS), and AS + Ech. Rats were administered AS (10 mg/kg) and Ech (1 mg/kg BW) by gavage for the experimental duration of 30 days. Ech inhibits oxidative stress by improving antioxidant levels, including glutathione, catalase, and glutathione-S-transferase, with a concomitant decrease in the amounts of malondialdehyde and nitric oxide in kidney and liver tissues. Moreover, it reduced blood concentrations of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, serum urea, uric acid, and creatinine. Concurrently, Ech resulted in a substantial increase in albumin and total protein levels. Additionally, Ech inhibits inflammation by reducing serum concentrations of tumor necrosis factor-α, cyclooxygenase 2, and prostaglandin E2.
CONCLUSION: Ech mitigates arsenic-induced hepatorenal damage by inhibiting oxidative stress and inflammatory pathways.