In recent years, individuals are rampantly exposed to vapours of benzene, through paint, plastic, petroleum industries, fuel exhaust, and tobacco smoke. Hence the present investigation was directed towards determining the effect of benzene metabolites, namely, phenol-hydroquinone and catechol, on the motility, viability, and nuclear integrity of the human spermatozoa. From the results obtained it was clear that exposure to phenol-hydroquinone caused a significant decline in both, sperm motility and viability. Exposure to a phenol-hydroquinone (Phase I) microenvironment may therefore inhibit metabolically active enzymes, thus impeding ATP production, and in turn lowers sperm motility and viability. In addition, the present study also revealed that both metabolites of benzene caused significant denaturation of sperm nuclear DNA. Hence, exposure to phenol-hydroquinone in vitro could have resulted in generation of free radicals and altered membrane function, which is reflected by a decline in the motility, viability, and loss of sperm nuclear DNA integrity. In Phase II, the exposure of human sperm in vitro to varied concentrations of catechol caused only insignificant changes in sperm motility and viability as compared to those observed on exposure to phenol-hydroquinone. Hence, exposure to catechol appeared to have less toxic effects than those of phenol-hydroquinone. 1. Introduction Benzene is an important industrial chemical present in petroleum products that is also omnipresent in the environment due to emissions from gasoline and combustion of hydrocarbons and tobacco [1, 2]. Urban populations throughout the world and cigarette smokers are routinely exposed to air concentrations of benzene in the range of 1–20？ppb [3]. Benzene is both exhaled unchanged in the lungs, as well as metabolized in liver and excreted as metabolites in the urine. The first step in benzene metabolism is the formation of benzene oxide, an epoxide, by cytochrome P-450 dependent mixed function oxidases. The epoxide undergoes hydroxylation to phenol which is then excreted as a glucuronidase or sulphate conjugate or converted to hydroquinone and benzoquinone. Phenol, hydroquinone glucuronide, and hydroquinone sulphate serve as markers for this enzymatic pathway. A second pathway involves conversion of benzene oxide to malondialdehyde through an NADPH mediated process, resulting in catechol production through the intermediate benzene glycol [4]. Significant concentrations of the phenolic compounds (phenol, catechol, and hydroquinone) are observed in human urine even in the absence of
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