Antioxidants are one of the key players in tumorigenesis, several natural and synthetic antioxidants were shown to have anticancer effects. The aim of the present study is to divulge the chemopreventive nature of carvacrol during diethylnitrosamine (DEN)-induced liver cancer in male wistar albino rats. Administration of DEN to rats resulted in increased relative liver weight and serum marker enzymes aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma glutamyl transpeptidase (γGT). The levels of lipid peroxides elevated (in both serum and tissue) with subsequent decrease in the final body weight and tissue antioxidants like superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx), and glutathione reductase (GR). Carvacrol supplementation (15 mg/kg body weight) significantly attenuated these alterations, thereby showing potent anticancer effect in liver cancer. Histological observations and transmission electron microscopy studies were also carried out, which added supports to the chemopreventive action of the carvacrol against DEN-induction during liver cancer progression. These findings suggest that carvacrol prevents lipid peroxidation, hepatic cell damage, and protects the antioxidant system in DEN-induced hepatocellular carcinogenesis.
Nowadays, in developing countries like India, incidence of lung cancer is increasing rapidly, and as a consequence it has become the most common cause of malignancy-associated death. This study is aimed to evaluate the therapeutic efficacy of beta-ionone (ION), a precursor for carotenoids against benzo(a)pyrene [B(a)P]-induced lung carcinogenesis. B(a)P (50 mg/kg body weight, orally twice a week for 4 successive weeks)-induced lung cancer in mice was assessed both in tissue and serum in terms of increase LPO and tissue marker enzymes, such as aryl hydrocarbon hydroxylase, γ-glutamyl transpeptidase, 5'-nucleotidase, and lactate dehydrogenase, and serum tumor markers such as carcinoembryonic antigen and neuron-specific enolase with concordant decrease in activities of tissue enzymic and non-enzymic antioxidants were observed on the treatment of ION (60 mg/kg body weight, orally twice a week for 16 weeks) significantly attenuated LPO and restored all cancer marker enzymes and antioxidants levels to near normal, which indicates the anticancer effect of ION. This was further confirmed by histological staining of argyrophilic nucleolar organizer region and histopathological analysis of lung tissue, immunohistochemical and immunoblot analysis of proliferating cell nuclear antigen. Overall findings suggested that the ION effectively ameliorated the lung carcinogenesis, which is attributed to the antiproliferative and antioxidant potential through free radical scavenging property.
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