Abstract
Hepatocellular carcinoma (HCC) is one of the most fatal cancers due to delayed diagnosis and lack of effective treatment options. Significant exposure to Aflatoxin B1 (AFB1), a potent hepatotoxic and hepatocarcinogenic mycotoxin, plays a major role in liver carcinogenesis through oxidative tissue damage and p53 mutation. The present study emphasizes the anticarcinogenic effect of Tridham (TD), a polyherbal traditional medicine, on AFB1-induced HCC in male Wistar rats. AFB1-administered HCC-bearing rats (Group II) showed increased levels of lipid peroxides (LPOs), thiobarbituric acid substances (TBARs), and protein carbonyls (PCOs) and decreased levels of enzymic and nonenzymic antioxidants when compared to control animals (Group I). Administration of TD orally (300 mg/kg body weight/day) for 45 days to HCC-bearing animals (Group III) significantly reduced the tissue damage accompanied by restoration of the levels of antioxidants. Histological observation confirmed the induction of tumour in Group II animals and complete regression of tumour in Group III animals. This study highlights the potent antioxidant properties of TD which contribute to its therapeutic effect in AFB1-induced HCC in rats.
Highlights
Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and accounts for around 70% of all liver cancers [1]
There was a significant increase in lipid peroxides (LPOs), thiobarbituric acid substances (TBARs), and Protein carbonyls (PCOs) in the HCC-induced (Group II) animals
The inhibitory effects of PCO by TD may be attributed to the presence of various bioactive components such as flavonoids, alkaloids, and polyphenols that act as antioxidants by scavenging chain-propagating, reactive free radicals generated by Aflatoxin B1 (AFB1)
Summary
Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and accounts for around 70% of all liver cancers [1]. Oxidative stress has emerged as a key player in the development and the progression of liver cirrhosis [4] which is known to be a precursor of HCC. Both hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be more potent in inducing oxidative stress, suggesting unique mechanisms that are activated by these viral infections. AFB1 is metabolized by cytochrome P450 enzymes to aflatoxin epoxide which is detoxified by the glutathione Stransferase system (GST) This reactive metabolite escapes from the detoxification process and usually conjugates with DNA nucleotides forming adducts [6]. G to T transversion mutations in codon 249 of the p53 tumour-suppressor gene have been found in human liver tumour from geographic areas with high risk of aflatoxin exposure and in AFB1-induced liver toxicity [8]
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