Pediatric obesity is closely associated with dyslipidemias and environmental factors, such as diet and lack of physical exercises, which may alter lipid profile in children. Rosuvastatin decreases serum total cholesterol and triglycerides concentrations. Vitamin C (ascorbic acid) plays an important role on sperm integrity and fertility. Juvenile male rats were distributed into six experimental groups that received saline solution 0.9%, 3 or 10 mg/kg/day of rosuvastatin, 150 mg/day of ascorbic acid, or 3 or 10 mg/kg/day of rosuvastatin co-administered with 150 mg/day of ascorbic acid from PND23 until PND53 and then the rats were maintained until sexual maturity. Rosuvastatin-exposed groups showed lower sperm quality, androgen depletion and germ cell death. Ascorbic acid was capable to prevent partially the reproductive adverse effects provoked by rosuvastatin. In conclusion, prepubertal exposure to rosuvastatin provokes long-term reproductive damages at sexual maturity and ascorbic acid supplementation at prepuberty may be a preventive mode against these reproductive adverse effects.

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Obesity during childhood and adolescence is closely related to dysfunctions on lipid profile in children. Rosuvastatin is a statin that decreases serum total cholesterol. Ascorbic acid is an important antioxidant compound for male reproduction. Pre-pubertal male rats were distributed into six experimental groups that received saline solution 0.9% (vehicle), 3 or 10 mg/kg/day of rosuvastatin, 150 mg/day of ascorbic acid, or 3 or 10 mg/kg/day of rosuvastatin co-administered with 150 mg/day of ascorbic acid by gavage from post-natal day (PND)23 until PND53. Rats were maintained until adulthood and mated with nulliparous females to obtain the male offspring, whose animals were evaluated at adulthood in relation to reproductive parameters. This study is a follow up of a previous paper addressing potential effects on F0 generation only (Leite et al., 2017). Male offspring from rosuvastatin-exposed groups showed increased sperm DNA fragmentation, androgen depletion and impairment on the testicular and epididymal structure. Ascorbic acid coadministered to the fathers ameliorated the reproductive damage in the offspring. In summary, paternal exposure to rosuvastatin may affect the reproduction in the male offspring; however, paternal supplementation with ascorbic acid was able to reduce the reproductive impairment in the male offspring caused by statin treatment to the fathers.

BackgroundOxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process. However, no study has compared different myocardial products of macromolecule oxidation after tobacco smoke exposure. Thus, the aim of this study was to investigate the lipid hydroperoxide (LH) levels, protein carbonyl concentrations and DNA damage in cardiac tissue of rats exposed to tobacco smoke.MethodsMale Wistar rats were divided into two groups: group C (control, n = 14) composed of animals not exposed to cigarette smoke; group ETS (exposed to tobacco smoke, n = 14) composed by animals exposed to cigarette smoke. The animals were exposed to 2 month of ETS and morphological, biochemical and functional analyses were performed.ResultsCardiac cotinine levels were elevated in the ETS group. In addition, the myocyte cross-sectional area was higher in the ETS group. (C = 266.6 ± 23.2 μm2 and ETS = 347.5 ± 15.1 μm2, p <  0.001). Cardiac LH was higher in the ETS group than in group C (C = 196.4 ± 51.5 nmol/g and ETS = 331.9 ± 52.9 nmol/g, p <  0.001). However, there were no between-group differences in cardiac protein carbonyl concentration or DNA damage.ConclusionsTherefore, our results suggest that, in this model, lipid damage is a good marker of oxidative damage during the cardiac remodeling process induced by 2 months of exposure to tobacco smoke.

SUMMARY:We evaluated the sperm parameters such as cauda epididymis weight, sperm count, sperm morphology and sperm DNA stability of adult CF-1 male mice treated daily (oral exposure) with the toxic sodium arsenite (As, 7.0 mg/kg/body weight); Melatonin (Me, 10.0 mg/kg/bw), Me (10.0 mg/kg/bw) plus As (7.0 mg/kg/bw) and Negative Control (NaCl 0.9%) to assess acute (8.3 days), chronic (33.2 days) and recovery of testicular damage (66.4 days). Arsenic decreases the number of sperm from chronic treatment (33.2 days) and this effect continued until 66.4 days of treatment. The toxic effect of As also altered the morphology of spermatozoa in all treatment periods when compared to the negative control group. However, Metalonin induced protective effects in periods of 33.2 and 66.4 days of treatment. Additionally, the stability of DNA was significantly affected by arsenic in all periods, but the chronic treatment (33.2 days) in the AsMe revealed increased stability compared to the group treated with arsenic only. Melatonin partially protects sperm toxicity caused by Arsenic, especially during periods of 33.2 and 66.4 days. 1252In this work, we aim to determine the effects of acute, chronic and recovery of testicular exposure to sodium arsenite in epididymal sperm and assess the use of melatonin as a protective agent and antioxidant. MATERIAL AND METHODThree-month-old male mice (Mus musculus) strain CF-1, healthy and sexually mature, were obtained from the Faculty of Medicine, University of Chile. The animals were maintained in a room under controlled conditions of temperature (22±2°C), and a 12 h light/dark cycle, with ad libitum access to commercial pellets and tap water.Reproductive changes were studied as acute (8.3 days), chronic (33.2 days) and recovery of testicular damage (66.4 days) in 88 adult mice exposed every day to oral doses of Sodium Arsenite (As; 7.0 mg/kg/bw, Sigma Chemical Co., St. Louis, MO); Melatonin (Me; 10.0 mg/kg/bw, Arama Laboratorios SA, Santiago, Chile) (Gutelkin et al., 2001); Me (10.0 mg/kg/bw) plus As (7.0 mg/kg/bw), and Negative Control (NaCl 0.9%) delivered orally in a volume not greater than 0.05 mL.Before the beginning and after the end of treatment, all animals were weighted. Euthanasia was performed by cervical dislocation after anesthesia with ketamine (Laboratory Biosano SA, Santiago, Chile) according to the protocol of animal handling of the Bioethics Committee of the Faculty of Medicine, University of Chile. Sperm Parameters.Extraction, weighing and sperm count in epididymalcauda. After obtaining the cauda epididymis they were weighed. Then sperm suspension was obtained using the protocol by Fornés & Bustos-Obregón (1994). Sperm were counted at 200X in a microscope, equipped to use Makler® chamber, adding a drop of sperm suspension by capillary and counting in duplicate the sperm present in the 100 squares of the camera, expressing this result as a million sperm/mg epididymis. Sperm morphology analysis.From the sperm suspension obtained above it was obtained 200 µL of sample. Addit...

Prenatal betamethasone (BM) exposure in rats negatively impacts sperm quality and male fertility. Studies have shown that BM can cause multi-generational effects on the pituitary-adrenal-axis of rats. The objective of this study was to assess the reproductive development and fertility of male rats (F2) whose fathers (F1) were exposed to BM (0.1mg/kg) on gestational days 12, 13, 18 and 19. In F2 rats, there was a significant reduction in body weights of the BM-treated group at PND 1 as well as delayed onset of puberty, and decreases in FSH levels, Leydig cell volume, sperm number and motility, seminal vesicle contractility and ejaculated volume. Furthermore, increased serum LH levels, sperm DNA damage and abnormal morphology were observed, resulting in reduced fertility. In conclusion, prenatal BM-treatment leads to intergenerational long-term reproductive impairment in male rats, raising concern regarding the widespread use of BM in preterm births.