Dietary Supplementation with D-Ribose-L-Cysteine Prevents Hepatic Stress and Pro-Inflammatory Responses in Male Wistar Rats Fed a High-Fructose High-Fat Diet.

Diets rich in fats and fructose are associated with the pathogenesis of oxidative stress-induced non-alcoholic fatty liver disease. Therefore, we investigated the effect of D-ribose-L-cysteine (DRLC) in high-fructose high-fat (HFHF) diet-fed rats. Twenty rats (n = 5), divided into four groups, were simultaneously exposed to HFHF and/or DRLC (250 mg/kg) orally during the 8 weeks of the study. Results showed that HFHF precipitated pro-inflammation and selective disruption of the oxidative stress markers. There were significant decreases in the level of antioxidants such as superoxide dismutase (SOD), glutathione peroxidase (GPX), total antioxidant capacity (TAC), hepatic SOD and GPX. Significant increases in serum levels of uric acid (UA), tumour necrosis factor-alpha (TNF-α), C-reactive protein (CRP) and hepatic Xanthine oxidase (XO) were observed in the HFHF compared to the control. In the HFHF + DRLC group, oxidative stress was mitigated due to differences in serum levels of SOD, GPX, TAC, TNF-α, liver SOD, and XO relative to control. The administration of DRLC alone caused significant reductions in malondialdehyde, UA and CRP and a significant increase in SOD compared to the control. DRLC prevents hepatic and systemic oxidative stress and pro-inflammatory events in HFHF diet-fed rats.

Acetonic extract of Vernonia amygdalina (Del.) attenuates Cd-induced liver injury: Potential application in adjuvant heavy metal therapy.

Exposure to cadmium (Cd), even at low doses, is of serious health concern because it does not undergo metabolic degradation to less toxic metabolite. Liver injury/disease, with a world-wide increasing incidence, is one of the consequences of exposure to Cd toxicity. This study aimed at determining the effects of acetonic extract of Vernonia amygdalina leaf (AEVAL) in a Wistar rat model of Cd-induced liver injury. Phytochemical screening of the extract was carried out and its oral LD50 was determined to guide the choice of therapeutic doses. Thereafter, thirty male Wistar rats were recruited for this study. The experimental groups received 4 weeks oral graded doses of the extract (100, 200 and 400 mg/kg) following Cd-induced liver injury. Cd-induced liver injury (5 mg/kg i.p for 5 consecutive days) was characterized by deleterious alterations in the levels of AST, ALT, ALP, total bilirubin and hepatic total protein (p ˂ 0.05). Also, deleterious alteration of oxidative stress indicators (GSH, SOD and CAT) and lipid peroxidation index (TBARS) was observed in the liver homogenates. Histopathological examination showed evidence of degenerated hepatocytes as well as inflammation with disseminated steatosis. These conditions were significantly attenuated (p ˂ 0.05) following treatment with graded doses of the extract, with the highest dose expressing least therapeutic effects. This study concluded that AEVAL attenuated Cd-induced liver injury and is, potentially, a suitable option in adjuvant therapy for heavy metal toxicity.