Parental ethanol consumption can influence the offspring phenotype. In this way, we analyzed the impairments of maternal and paternal high ethanol consumption during postpuberty on the physical development, feeding pattern, puberty onset and reproductive function of ethanol-naive offspring to birth to adulthood. Female and male UChB rats (voluntary 10%, v/v ethanol consumer) were divided into a control group (C) and an ethanol exposed group (E) from 65 to 80 days of age. The C and E were mated at 100 days. The maternal parameters and offspring development and reproduction parameters were monitored. We observed reduced feeding intake and body weight in the dams of E group throughout gestation and lactation period. Delay in physical development, lower body weight and altered feeding pattern were observed in female and male offspring of E group. In addition, the puberty onset was delayed in both sexes, with lower testosterone levels in the juvenile and pubertal males. There was a prolongation on the estrous and proestrus phases in females from E but the estrous cycle duration did not change between groups. Ovary and uterus weight were reduced in pubertal and adult females from E group. Reduced epididymis and seminal vesicle weight, increased sperm abnormalities, decrease in the daily sperm production and accelerated epididymal transit time were observed in E males. The high maternal and paternal ethanol use on postpuberty impairs the parameters of ethanol-naive offspring inducing alteration on development and reproduction.

Male infertility is responsible for 20-70% of infertility in couples. We investigated the effects of fetal programming with sodium saccharin consumption in testis structure and function and in male offspring fertility. Feed intake and efficiency, organ and fat weight, quantification and expression of AR and PCNA proteins, sperm count and hormonal dosages were performed. Changes in consumption were found in the final weeks of the experiment. Decreases in the expression and quantification of AR and PCNA, tubular diameter and luminal volume, and increase in epithelial and interstitial relative volumes were observed. Lower sperm count and transit and lower estradiol concentration were also found. The consumption of sodium saccharin by the dams programmed the male offspring affecting the HPG axis with alterations in Sertoli cell proliferation, AR expression and quantification, and sperm count. We hypothesize that these changes may be due to the reduction of estradiol that caused the loosening of the tight junctions of the blood-testis-barrier (BTB), causing cell losses during spermatogenesis, also reflecting, under the decrease in tubular diameter with an increase in epithelial volume and consequent decrease in luminal volume. Sodium saccharin programming directly affected the reproductive parameters of male offspring and adult fertility.

The relationship between adolescent ethanol uses and its impacts throughout life are not conclusive. Thus, we evaluated if the low and high consumption of ethanol at postpuberty interferes with the reproduction, ethanol-naive offspring and if the effects are dose-related. Female and male rats were divided into three groups: low drinker (L), high drinker (H), and control (C). The L and H groups were exposed to ethanol to 10% from 65 to 80 days with withdrawal after this period. The ethanol consumed by low drinkers was 1.41 ± 0.21 g/ kg / day and high drinkers 4.59 ± 0.45 g/ kg / day. The study was conducted in two phases. The 1st phase verified the reproductive capacity in adulthood on generations (litter size and sex ratio). Data were collected over ten years. The 2nd phase analyzed the parent reproductive parameters (body weight, reproductive organ weight, sperm parameters and estrous cycle) and the pup development. We observed a reduced litter size in both drinker groups. Gestational body weight gain and feed consumption were lower in L and H. We observed an alteration in reproductive organs weight in both sexes of H. Females presented a longer estrous cycle duration. Males presented an increase in abnormal sperm, a decrease in sperm count and accelerated transit time. The ethanol-naïve offspring development was also impaired. We conclude that low and high postpubertal alcohol use impairs long-term reproductive parameters, even after alcohol withdrawal. There is also impaired ethanol-naive offspring. Besides, the effects are dose-related.

Background Despite the absence of scientific data supporting the real impact of drinking on elderly individuals, alcohol abuse is a common feature of older people. Because aging is associated with biological changes that include reduced water volume in the body, lower efficiency of liver enzymes and hepatic blood flow, and altered brain responsiveness due to drug interactions, elderly individuals are more prone to the harmful effects of alcohol consumption. The adverse effects of acute or chronic exposure to ethanol have been extensively recognized on cerebellar circuits, with impairment in movement and balance. In addition to motor deterioration, cerebellar degeneration contributes to distinct neuropsychological deficits in chronic alcoholics and children with prenatal exposure to ethanol. However, the effects on senile individuals are unclear. This study determines the pattern of MicroRNAs, gene expressions, apoptotic and anti-apoptotic protein levels, and ultrastructural analysis of neurons to contribute to the understanding of the consequences of alcohol abuse on the senile cerebellum.Methods and Results The results of immunohistochemical and gene expressions for Caspase-3, XIAP, and IGFR-1 were similar in both groups. Serum levels of miR-9-3p, -15b-5p, -16-5p, -21, − 200a, and − 222-3p were upregulated in the presence of ethanol with aging.Conclusions The results suggest an important tolerance development by the UChB rats to chronic ethanol consumption in the aged cerebellum, and miRNAs may be potentially involved with this mechanism.