The objective of this study was to assess the toxicological effect of exposure to benzo(a)pyrene, B[a]P, on germ cells during spermatogenesis. Mice were exposed to B[a]P at 1, 10, 50, and 100？mg/kg/day for 30 days via oral ingestion. Germ cells, including spermatogonia, spermatocytes, pachytene spermatocytes, and round spermatids, were recovered from testes of mice exposed to B[a]P, while mature spermatozoa were isolated from vas deferens. Reproductive organs were collected and weighed. Apoptotic response of germ cells and mature spermatozoa were qualified using the terminal deoxynucleotidyl transferase mediated deoxy-UTP nick end labeling (TUNEL) assay. B[a]P exposure at ≤10？mg/kg/day for 30 days did not significantly alter concentrations of germ cells and mature spermatozoa and apoptotic response in germ cells and mature spermatozoa. Exposure to B[a]P at 50 and 100？mg/kg/day induced testicular atrophy and yielded a significant reduction in the concentrations of spermatogonia, spermatocytes, pachytene spermatocytes, and round spermatid cells as compared with the control. Also, mature spermatozoa experienced decreased concentrations and viability. B[a]P-exposed mice experienced a significant increase in apoptotic germ cells as compared to the control mice. However, the mice dose concentrations were not relevant for comparison to human exposure. 1. Introduction Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon compound, is produced by incomplete combustion of organic compounds and high-pressure processes. This compound is commonly present in motor vehicle exhaust, tobacco smoke, grilled, smoked and broiled foods, and emissions from residential and industrial heating sources. Biotransformation of B[a]P occurs as it undergoes initial oxidation by cytochrome P450 enzymes and consequently forms reactive metabolites, for example, B[a]P-9, BaP-7,8-dihydrodiol 9,10-epoxide and quinones. The active intermediates are capable of covalently bonding to DNA [1] and form DNA adducts. Also, they can undergo redox cycling and generate excessive reactive oxygen species, which may alter cell signaling and damage cellular membranes resulting in apoptosis [2]. Previous studies in animal models have demonstrated that direct exposure to B[a]P could cause toxic effects on male reproduction and has been implicated in the pathobiology of adverse reproductive health. B[a]P has been related to decreased spermatozoa quality [3, 4] and germ cell apoptosis after chronic exposure [5]. To date, limited data has appeared available to depict the impact of exposure to B[a]P on
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