There are a large number of agricultural workers who are exposed to pesticides through skin and inhalation. The best approach to identify altered molecular pathways during dermal exposure to pesticides is relevant to risk-associated concern about skin safety. In this study, we investigated the cytotoxic effect of zineb, a fungicide, in human keratinocyte (HaCaT) cells. HaCaT cells were treated with zineb (1–40 µg/mL) for 24 hours. Cellular and molecular mechanisms of cell toxicity were investigated through MTT and neutral red-uptake assays. Zineb reduced viability of HaCaT cells and induced apoptosis in a concentration-dependent manner. Zineb increased levels of Bax and caspase 3 and inhibited the level of Bcl2, which subsequently induced apoptosis via the Bax/Bcl2 and caspase pathway. Therefore, zineb could have induced apoptosis through the mitochondrial pathway in HaCaT cells. Our study suggests that zineb is cytotoxic to HaCaT cells via the induction of apoptosis and oxidative stress in vitro.

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ObjectiveOral precancerous lesions like oral leukoplakia and oral submucosal fibrosis are very common in north Indian population which often leads to oral squamous cell carcinoma. Chewing of tobacco, pan masala, and betel nut is very common among north Indian women. Reactive oxygen species (ROS) generation is an important outcome of this habit. Imbalance between ROS and antioxidants leads to oxidative stress. The aim of our study was to determine the level of antioxidants in oral precancerous lesions and oral cancer to predict disease susceptibility.MethodThe study group consisted of 120 subjects among which 25 were with histopathologically confirmed oral cancer, 50 with histopathologically confirmed oral precancerous lesions, and 45 were healthy controls. Blood samples were collected for the evaluation of reduced glutathione (GSH) and antioxidant enzymes, catalase, superoxide dismutase (SOD), glutathione reductase (GR) and oxidative stress markers like malondialdehyde (MDA) and nitrite.ResultResults demonstrated a decrease in antioxidant enzymes such as catalase, SOD, and GR in oral precancerous lesion and oral cancer from that of healthy control. An increase in reduced glutathione concentration was observed in oral precancerous lesion and oral cancer as compared to healthy control. Malondialdehyde level was increased significantly in oral cancer. Increase in nitrite concentration was not statistically significant in oral precancerous lesion and oral cancer patients as compared to control.ConclusionOxidative stress and antioxidants have been found to be important indicators in oral cancer and in pre‐malignant lesions which may predict susceptibility of development of oral cancer.

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IntroductionOral cancer is one of the most common cancers in Northern India. Carcinogenic substances found in cigarette or tobacco can cause inflammation of the lining of oral cavity and pathogenesis of oral cavity cancer. Tumor necrosis factor is a pro‐inflammatory cytokine involved in the immunoinflammatory diseases. The aim of this research was to determine the impact of smoking and tobacco chewing and polymorphism in TNFα −238 G/A and TNFα −308 G/A, on the risk to precancerous oral lesions and oral cavity cancer.MethodsGenotyping was done by polymerase chain reaction and restriction fragment length polymorphism method in 75 patients with oral cavity cancer, 75 patients confirmed with precancerous lesions, and 100 controls.ResultsTNFα −238 G/A SNP was not associated with the risk of oral precancerous lesions or oral cavity cancer. TNFα −308 G/A was strongly associated with precancerous lesions and oral cancer. No correlation was found between smoking or tobacco chewing habits and TNFα −238 and TNFα −308 G/A polymorphism with oral precancerous lesions and oral cavity cancer.ConclusionThe study shows no significant interaction between smoking or tobacco chewing habits and polymorphism in TNFα −238 and TNFα −308 G to A with precancerous lesions and oral cancer although TNFα −308 G/A was strongly associated with precancerous lesions and oral cancer.