Ganoderma lucidum protects liver mitochondrial oxidative stress and improves the activity of electron transport chain in carbon tetrachloride intoxicated rats.

AIM: Liver injuries induced by carbon tetrachloride (CCl(4) ) cause mitochondrial stress and disruption of membrane potential resulting in apoptosis. In this study, we evaluated the effects of Ganoderma lucidum against CCl(4) (1:5 v/v in paraffin oil, 1.5 mL/kg, i.p) induced deterioration of the activities of mitochondrial enzymes and electron transport chain complexes in the liver mitochondria.
METHODS: Ganoderma lucidum (100 and 250 mg/kg) was administered once daily for 15 days prior to the CCl(4) administration. α-Tocopherol (100 mg/kg, p.o.) was used as the standard. Hepatic damage was assessed by determining the activities of serum transaminases (SGPT and SGOT) and alkaline phosphatase (ALP), 24 h after CCl(4) injection. The activities of mitochondrial dehydrogenases as well as mitochondrial complexes I, II, III, and IV were evaluated.
RESULTS: Activities of SGPT, SGOT and ALP were significantly (P < 0.01) elevated whereas, the activities of mitochondrial enzymes were significantly (P < 0.01) decreased by the CCl(4) challenge. The mitochondrial reactive oxygen species level was enhanced and mitochondrial membrane potential was declined significantly. Administration of G. lucidum significantly and dose independently protected liver mitochondria.
CONCLUSION: The findings suggest that protective effect of G. lucidum against hepatic damage could be mediated by ameliorating the oxidative stress; restoring the mitochondrial enzyme activities and membrane potential.