The report compares the statistical precision and biological sensitivity of multiple indicies of reproductive function to infertility in the male rodent. The studies discussed include those that examined reproductive function in the male following perinatal exposure to reproductive toxicants and others in which the compounds were administered to young-adult males, often with very diverse results. For example, some chemicals that alter sex differentiation reduce fertility by affecting breeding performance alone (PCBs, fenarimol, or losulazine), without altering sperm and testicular measures. Others also markedly alter sex differentiation of the genitalia, the accessory glands and the testis in addition to their effects on CNS sex differentiation and mating behavior (testosterone, flutamide, cyproterone acetate, tamoxifen, estradiol and DES). In contrast, prenatal exposure to compounds that alter primary germ cell survival (busulphan, congo red) induce partial gonadal germ cell agenesis without altering sex differentiation. These chemicals dramatically reduce testicular sperm production in the male offspring and the most severely affected males are infertile. Young male rats were exposed to known reproductive toxicants in a dose related manner from puberty, through young adulthood and breeding. It was found that the profile of effects varies considerably depending upon the chemical's mechanism of toxicity. When a compound produced infertility through direct effects of testicular function (MBC and DBP), then testis weight, testicular histology and testicular sperm head counts provided sensitive indicators of toxicity.