The Chronic Elevated Consumption of Hibiscus sabdariffa Linnaeus Results in Kidney Damage Associated with Excess H2S

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Abstract

Hydrogen sulfide (H2S) is essential for renal function; however, it is toxic at high concentrations. H2S is increased during reductive stress (RS). Increased antioxidant capacity and reduced/oxidized glutathione (GSH/GSSG) characterize a rat model of RS associated with chronic consumption of 6% Hibiscus sabdariffa Linnaeus (HSL). Here, we evaluate if chronic consumption of an infusion of HSL causes kidney damage associated with an increase in H2S. Twenty-one Wistar rats were divided into three groups. Group 1: rats received plain tap water ad libitum (G1); Group 2: rats received an ad libitum infusion of 6% HSL for one month (G2); and Group 3: rats consumed a 6% HSL infusion for one month and were then given natural water for another month (G3). We evaluated renal vasodilatation, cystathionine–β–synthase (CBS), cystathionine–γ–lyase (CSE), 3–mercaptopyruvate-sulfur-transferase (3–MST), γ-glutamylcysteine synthetase (GCLC), Nrf2, total OXPHOS, H2S concentration, GSH/GSSG and oxidized/reduced thiols in the kidney. Renal vasodilatation and total OXPHOS in complex IV and I and oxidized/reduced thiols were decreased (p ≤ 0.01) but H2S, CBS, SCE, GCLC, and NrF2 expression and GSH/GSSG were increased (p ≤ 0.04). The HSL infusion provided cysteine that was metabolized by CBS and CSE, elevating chronic H2S and favoring renal damage.

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