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.