Testicular germ cell tumour is the most common malignancy in young males and its incidence has been rising in recent years. Environmental and occupational exposures are believed to increase the risk of testicular cancer. The exposures along with genetic susceptibility may influence the risk of developing Testicular germ cell tumour even further. Phthalates are endocrine disruptors and are abundantly used as industrial plasticisers. Human exposure to phthalates occurs from the use of this substance in commerce. Di-2-(ethylhexyl) phthalate (DEHP) is the most common phthalate found in consumer products. Post exposure DEHP is rapidly hydrolysed into its active form, mono-(2-ethylhexyl) phthalate (MEHP), a testicular toxicant and a carcinogen. The objective of this research was to determine the toxicity of MEHP. Possible mechanisms that may be involved in the pathogenesis of testicular atrophy from exposure to MEHP include FAS signalling, ROS signalling, NF-kB, PPAR and cAMP pathway. Alternative mechanisms may also be associated with the regulation of germ cell apoptosis leading to testicular atrophy. Relevant genes of interest that may be affected are Testisin, GSTP1, and MGMT. The expression of these genes was examined by RT-PCR in testicular germ cells exposed to MEHP in a dose- and time-dependent manner at concentrations of 1 μM, 10 μM, and 100 μM at 24, 48, 72 and 96 h time points. The findings of this study will allow for a better understanding of the role of phthalates in altering expressions in testicular germ cells and a better understanding of the process of testicular carcinogenesis.
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