Fruits and vegetables contain a variety of ingredients that exhibit chemopreventive effects against an array of xenobiotics. In the present study, the antigenotoxic potential of lupeol, a triterpene, and mango pulp extract (MPE) was evaluated in Swiss albino mice. Benzo[a]pyrene (B[a]P), a well-known mutagen, was given at a single dose of 100 mg/kg body weight intraperitoneally. Pretreatment with lupeol (1 mg/animal) and MPE (1 mL, 20%) was given through oral intubation for 7 days prior to B[a]P administration. Animals from all the groups were killed at sampling time of 24 h and their bone marrow tissue was analyzed for chromosomal damage and micronuclei induction. In B[a]P-treated animals a significant induction of chromosomal aberration and micronuclei was recorded, with a decrease in mitotic index. In lupeol- or MPE-supplemented groups, a significant decrease in B[a]P-induced clastogenicity was recorded. The incidence of aberrant cells and micronuclei was found to be reduced by both lupeol and MPE when compared to the B[a]P-treated group. The anti-cytotoxic effects of lupeol or MPE were also evident, as observed by significant increase in mitotic index. Thus, results of the present investigation revealed that lupeol and MPE have protective effects against B[a]P-induced clastogenic changes in Swiss albino mice.
The present case‐control study aimed to investigate the role of interaction of glutathione‐s‐transferase (GST) genotypes with environmental risk factors in determining susceptibility to head and neck squamous cell carcinoma (HNSCC) involving 1,250 cases and equal number of healthy controls. An increase in the risk of HNSCC and its subsites (larynx, pharynx, and oral cavity) was observed among the cases with null genotypes of GSTM1 (odds ratio [OR] = 1.87) or GSTT1 (OR = 1.39) while reduced risk (OR = 0.81) was observed the cases with variant genotype of GSTP1. Tobacco use in the form of smoking or chewing interacted multiplicatively with GSTM1 or GSTT1 to increase the risk several folds (3–10 folds) in HNSCC and its subsites. Alcohol use also increased the risk (2–3 folds) to HNSCC and its subsites in cases with null or variant genotypes of GSTs, though this risk was of lesser magnitude when compared to the tobacco users. A synergistic effect of both, tobacco smoking and alcohol drinking, led to several folds (25‐folds) increased risk to HNSCC among the cases with null genotype of GSTM1 and GSTT1 when compared to nonsmokers and nondrinkers with wild genotype of GSTM1 and GSTT1 in controls. Furthermore, cases with variant genotypes of GSTP1 (Val/Val) showed superior treatment response with improved survival rate and lower risk of death when compared to the patients with wild type genotype (Ile/Ile). The data suggest that though polymorphism in GSTs may be a modest risk factor for determining HNSCC risk, gene‐environment interactions significantly modify the susceptibility to HNSCC by several folds.
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