Effects of prenatal and lactation nicotine exposure on rat testicular interstitial tissue

Nicotine is largely consumed as a component of cigarettes. It induces apoptosis, interferes with endocrine function by changing the sex hormones secretion and leads to male infertility. Testosterone is produced from cholesterol by Leydig cells (LC), with the participation of testicular macrophages (MO). Thus, to investigate whether nicotine administration to pregnant and lactating rats changes cholesterol and sexual hormone levels and LC and MO populations of offspring, female rats received nicotine (2mg/kg/day) through osmotic minipumps from the first day of pregnancy up to the end of weaning. At 1, 30, 60 and 90days post-partum (dpp) the plasma cholesterol and testosterone levels were obtained, as well as the biometric, histopathological and stereological testicular parameters. Nicotine reduced the body weight, cholesterol levels and lipid droplet number in foetal LC at 1dpp. The number of apoptotic LC did not change in the offspring of nicotine group at any age studied. No alterations in the numerical densities of MO and LC occurred at 60 and 90dpp. Hypertrophy of mature LC and increase in cholesterol and testosterone levels were noted at 90dpp. In conclusion, nicotine when administered to rats throughout pregnancy and lactation induces morphofunctional alterations of foetal and mature LC and affects cholesterol and testosterone levels.