Peripubertal paternal EtOH exposure - Testicular oxidative injury, fecundity, and offspring

Fetal alcohol syndrome usually implies effects on the offspring of maternal EtOH consumption during gestation, with fewer reports addressing the impac t of paternal-exposure on the progeny. One previous report has dealt with t he impact of EtOH exposure on peripubertal male rats as a model of teenage drinking and the deleterious effects on the offspring. We report here findi ngs examining the effect of 2 mo of EtOH feeding on male animals as they pr ogressed through puberty on their ability to impregnate EtOH-naive female r ats and characteristics of the subsequent litters. The EtOH-imbibing father s weighed significantly less than pair-fed controls and animals ingesting a non-EtOH liquid diet ad libitum, Nevertheless, they were able to mate succ essfully, although fecundity was significantly reduced. The number of succe ssful pregnancies, defined as carried to term, was diminished from 92% in c ontrols to 75% in EtOH-fed animals (p < 0.05), There was increased paternal testicular oxidative injury demonstrated by enhanced lipid peroxidation, p rotein oxidation, and decreased ratio of reduced to oxidized glutathione, T he litter size of the EtOH-exposed males was reduced by 46%, The average li tter size was 12.4 +/- 1.5 pups/litter in ad libitum animals, virtually ide ntical to the 12.5 +/- 0.6 pups/litter in the pair fed controls. This is in sharp contrast to the 6.7 +/- 0.1 pups/litter from the paternal EtOH matin gs (p < 0.001), There was an increase in the average individual weight of p up offspring of paternally EtOH-exposed animals (p < 0.01 vs pair-fed contr ols and p < 0.05 vs ad libitum), Curiously, the male-to-female pup ratio wa s altered with a higher preponderance of male offspring from EtOH-fed fathe rs. There were no gross malformations noted among the pups, Insulin-like gr owth factor-1 levels in the pups at 10 d of age were unaltered between the groups. However, leptin was significantly elevated in the EtOH offspring. I t appears that chronic EtOH exposure in the peripubertal fathers subsequent ly decreases fecundity and that this may be mediated by testicular oxidativ e injury, perhaps leading to accelerated germ cell apoptosis.