NNK (4-(methylnitrosamino)―1-(3-pyridyl)-1-butanone) is a major form of nitrosamine abundant in cigarette smoke and is a powerful carcinogen. Mercury is a major component of the amalgam that is widely used as dental filling material. Concurrent exposure to these two agents may result in their interaction and alter their carcinogenic potential. The present study used an immortalized human epithelial cell system that allows continuous exposure to potential carcinogens, in an attempt to elaborate the carcinogenic potential of mercury and NNK in humans. Cytotoxicity of mercury chloride and NNK was measured by an MTT assay. Parameters of neoplastic cellular transformation such as cell saturation density, soft-agar colony formation, and cell aggregation were analyzed to examine the carcinogenic potential of mercury chloride and NNK. The study showed that exposure to mercury chloride with NNK resulted in increased soft agar colony formation and cell aggregation. ROS generation by mercury chloride was further enhanced by treatment with NNK. The apoptosis that was observed following mercury chloride exposure was further increased upon co-treatment with NNK. The interaction between these two agents was also observed in cytokine mRNA induction. In the present study, mercury alone did not seem to pose a significant threat as a carcinogen, but it may have potential to enhance the carcinogenic potential of a known carcinogen from cigarette smoke. The present study provides valuable data regarding the evaluation of potential carcinogenic risk of mercury chloride and NNK on concurrent exposure.
Germination and early elongation of rice after germination were investigated in anoxic air treatment, nitric oxide gas treatment, and six concentrations of mercuric chloride solutions to determine the effects of limited oxygen environment, nitric oxide, and inhibited water flux through cell membrane in 17~circC . Anoxic air treatment affected germination of tested six varieties very little. However root elongation rates were severely inhibited while shoot growth was affected less. Reductions in shoot and root elongations demonstrated genotypic variations. Nitric oxide delayed the germination of rice even though it didn't affect the final percent germination. Elongations of root and shoot were inhibited in nitric oxide treatment. The inhibitor effect of nitric oxide on the shoot elongation of rice was less severe, while nitric oxide completely inhibited the root emergence of rice. Concentrations of HgCl2 greater than 300~muM dramatically reduced the rate and percentage of germination when compared to distilled water treatment. The reduced percent germination showed the greatest variation among rice varieties in 500~muM solution of mercuric chloride. Ansanbyeo, Jinheung, and Odaebyeo were affected less by HgCl2 , Nonganbyeo and Sangmibyeo were intermediate, and the germination of Andabyeo was greatly reduced by HgCl2 . Root elongation of germinated rice seedlings was more sensitive to oxygen deficits, nitric oxide, and HgCl2 treatments than germination and shoot elongation. In conclusion, poor seedling establishment of rice sown in flooded paddy soils, in which the oxygen supply to the seeds is restricted, appears to the result of limited root elongation rate.
Mercuric chloride, inorganic compound, is one of the most important drugs that has been used in the field of argriculture, antisyphilitica and anticeptics, but it is not used clinically at present. We have studied the effect of testosterone on the mercuric chlorideinduced nephrotoxicity. Renal lipid peroxide concentration of male rat treated with mercuric chloride was significantly increased in comparison with that of the female rat, it showed similar effects on testosterone pretreatment. Changes in renal catalase and glutathione peroxidase activities were not siginificantly different in testosterone-treated groups. But, renal xanthine oxidase and aldehyde oxidase activities of testrosterone-treated group given mercuric chloride significantly increased in comparison with that of the testosterone-treated alone. Animals treated with testosterone prior to mercuric chloride showed more severe damage on histological observations than those treated with testosterone only. Consequently, we suggest that the mercuric chloride-induced nephrotoxicity might be renal lipid peroxide generating enzyme system by testosterone.