ABSTRACT
Background: Cancer is the second most common fatal disease in the world, behind cardiovascular disorders in the first place. It accounts for around 0.3 million deaths per year in India due to the lack of proper diagnostic facilities, prevention and treatment. Current therapeutic methods do not provide adequate protection and affect normal cells along with cancerous ones. Thus, there is a need for some alternative therapeutic strategy, preferably from natural products, which have been traditionally used for treatment of various diseases in the country. Methods: In this study, we have conjugated purified NN-32 toxin from Naja naja venom with gold nanoparticles and its anticancer potential was evaluated against human breast cancer cell lines. UV-Vis spectroscopy, dynamic light scattering, transmission electron microscopy, atomic force microscopy and zeta potential analysis were the techniques used for characterization of GNP-NN-32. Results: GNP-NN-32 showed dose- and time-dependent cytotoxicity against breast cancer cell lines (MCF-7 and MDA-MB-231). NN-32 and GNP-NN-32 induced apoptosis in both breast cancer cell lines. The results of CFSE cell proliferation study revealed that NN-32 and GNP-NN-32 arrested cell division in both MCF-7 and MDA-MB-231 cell lines resulting in inhibition of proliferation of these cancer cells. Conclusion: GNP-NN-32 showed an anticancer potential against human breast cancer cell lines. Analysis of detailed chemical characterization along with its cytotoxic property might help to perceive a new dimension of the anti-cancer potential of GNP-NN-32 that will enhance its biomedical function in near future.(AU)
Subject(s)
Animals , Elapid Venoms , Naja naja , Antineoplastic AgentsABSTRACT
Industrial, domestic and agricultural wastes pose potential threat to the aquatic environment as major sources of toxic contaminants along with carcinogenic and genotoxic compounds. Heavy metals and polycyclic aromatic hydrocarbons (PAH) have increased concern due to their mutagenic features as they can bind to DNA molecule and lead to genotoxicity. In the present study, we evaluated the genotoxic potential of cupric chloride di-hydrate (A), anthracene (B) and combined exposure of both (C) on the freshwater mussel, Lamellidens corrianus (Lea 1834). Animals were exposed individually to cupric chloride di-hydrate (A, 0.1 ppm) and anthracene (B, 0.5 ppm) and their combined exposure (C) for 7 days (T1) and 14 days (T2), followed by the transfer of exposed animals to toxicant free water for four days after each treatment for assessment of recovery pattern (R1, R2). Genotoxicity was evaluated after each exposure and recovery with the help of comet assay and micronucleus assay. In all the above exposures (A, B and C) it was observed that increased exposure duration leads to more DNA damage. However, recovery potential of animals upon exposure to extended duration found to be greater than that of the short duration exposure (R2>R1), indicating adaptability of animals. The trend of damage in tail DNA% and olive tail moment (OTM) was consistent after both (T1 and T2) durations such as C>A>B.
ABSTRACT
Monocrotophos (MCP) is an organophosphate pesticide widely used in India for controlling various pests. In this study, we evaluated the oxidative stress and genotoxic potential of MCP on the freshwater mussel Lamellidens marginalis (Lamarck) after 7 days exposure and repair of the damaged DNA after 4 days recovery. The bivalves were exposed to 5.25 mg/L of MCP for 7 days and then allowed to recover for 4 days in pesticide-free water. Increase in the levels of thiobarbituric acid reactive substances was recorded in the gill, muscle, foot and mantle tissues. Cellular antioxidant defences i.e. antioxidant enzyme activities like catalase, superoxide dismutase, glutathione reductase and glutathione-S-transferase were used as biomarkers of oxidative stress. Altered activities of antioxidant enzymes were observed after exposure. There was a significant recovery in the antioxidative enzymes in the tissues after the recovery period. To monitor genotoxicity of MCP, we used micronucleus and comet assay. Increase in Olive tail moment in the gill cells of exposed mussels as compared to that of control ones indicated significant DNA damage. Our findings suggest that the MCP-induced oxidative stress may be contributing partly to genotoxic damage of gill cells. Thus, these biomarkers are found to be useful in evaluating the toxicity of MCP in mussels.