Purpose: Phenobarbital is a commonly employed antidepressant and anti-epileptic
drug. The cancer promoting activity of this genotoxic xenobiotic is often ignored. It is
responsible for oxidative stress leading to modulation in xenobiotic and antioxidative enzymes.
Glucosinolates and more specifically their hydrolytic products are known for their antioxidative
and anticancer activities. The present study involves the analysis of hepatoprotective effect of
erucin (isolated from Eruca sativa (Mill.) Thell.) against phenobarbital mediated hepatic
damage in male wistar rats.
Methods: The liver homogenate was analyzed for oxidative stress (superoxide dismutase,
catalase, guaiacol peroxidase, ascorbate peroxidase, glutathione reductase and lactate
dehydrogenase), other oxidative parameters (thiobarbituric acid reactive species, conjugated
dienes and lipid hydroperoxide), phase I enzymes (NADPH-cytochrome P450 reductase,
NADH-cytochrome b5 reductase, cytochrome P420, cytochrome P450 and cytochrome b5),
phase II enzymes (γ-glutamyl transpeptidase, DT-diaphorase and glutathione-S-transferase), serum parameters
(alkaline phosphatase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, direct bilirubin
and total bilirubin) and certain histological parameters.
Results: Erucin accorded protection from phenobarbital induced hepatic damage by normalizing antioxidative
enzymes, other oxidative parameters, phase I, II, and serum parameters.
Conclusions: Erucin, an analogue of sulforaphane has the potential to act as an anticancer agent by regulating various