Kumar S, Antony M, Mehrotra N K
Laboratory Industrial & Environmental Carcinogenesis, Industrial Toxicology Research Centre, Lucknow, India.
Arch Dermatol Res. 1988;280(6):371-4. doi: 10.1007/BF00426616.
The role of glutathione (GSH) in skin tumor promotion was ascertained in the present study by investigating the effect of the GSH depletor, diethyl-maleate (DEM), on the tumor-promoting ability of TPA in DMBA-initiated mouse skin. DEM lowered the tumor yield and the tumor incidence by 80% (p less than 0.001) in the DMBA + TPA treated group. The rate of tumor formation was also found to be influenced by DEM. The results suggest that clonal expansion of tumor-initiated cells, stimulated by TPA, depends upon the availability of reduced GSH in the tissue. The mechanism by which depletion of reduced GSH could result in inhibition of skin tumor promotion is not known. However, inactivation of GSH and thus blockage of the physiological function of reduced GSH in the biochemical events obligatory to tumor-cell proliferation in mouse skin could be the possible mechanisms providing effective control over proliferation of tumor cells.
本研究通过调查谷胱甘肽（GSH）消耗剂马来酸二乙酯（DEM）对二甲基苯并蒽（DMBA）引发的小鼠皮肤中佛波酯（TPA）促肿瘤能力的影响，确定了GSH在皮肤肿瘤促进中的作用。在DMBA + TPA处理组中，DEM使肿瘤产量和肿瘤发生率降低了80%（p < 0.001）。还发现肿瘤形成速率受DEM影响。结果表明，由TPA刺激的肿瘤起始细胞的克隆扩增取决于组织中还原型GSH的可用性。还原型GSH耗竭导致皮肤肿瘤促进受抑制的机制尚不清楚。然而，GSH的失活以及因此在小鼠皮肤肿瘤细胞增殖所必需的生化事件中还原型GSH生理功能的阻断可能是对肿瘤细胞增殖提供有效控制的可能机制。
