Background: Formaldehyde (FA) is one of the most widely used materials in industries and in sciences. Prolonged contact with FA might have harmful effects on fertility due to the increase in the reactive oxygen species level. On the other hand, date palm (Phoenix Dactilifera L.) fruit extract (DPFE) contains a high concentration of natural antioxidants that could scavenge free radicals. Objective: The aim was to investigate the prophylactic effects of DPFE, with strong antioxidant properties, on FA-induced testicular toxicity in male mice. Materials and Methods: Thirty-two adult NMRI male mice with a weight range of 25- 35 gr (9-10 wk old) were randomly divided into four groups: control group (distilled water, orally for 35 days), FA group (FA; 0.25 mg/kg intraperitoneally (i.p.) for 20 days), treatment group (Date (DT) + FA; DPFE, 4 mg/kg for 35 days followed by FA administration, 0.25 mg/kg, i.p., for 20 days), date fruit extract group (DT; DPFE, 4 mg/kg, orally for 35 days). After this, blood was collected and left epididymis and testis tissues were isolated to evaluate the sperm parameters and histological examination, respectively. Results: The FA administration increased the sperm morphological anomalies and reduced the sperm count, viability and motility, and also testosterone compared to the control group (p ≤ 0.001). In addition, histological studies of the testes showed that FA causes changes in the testis seminiferous tubules such as destruction of germinal epithelium and vacuolization of the tubules. The DPFE consumption before FA administration could partially ameliorate the reduced testosterone, sperm, and testicular parameters due to FA. Conclusion: The DPFE use might have discount effects on FA-induced testicular toxicity. Key words: Formaldehyde, Date fruit, Testis, Toxicity, Sperm, Testosterone.

Autism spectrum disorder is a neurodevelopmental disorder characterized by deficits in social communication and repetitive behavior. Many studies show that the number of cognitive impairmentscan be reduced by antagonists of the histamine H3 receptor (H3R). In this study, the effects of ciproxifan (CPX) (1 and 3 mg/kg, intraperitoneally) on cognitive impairments in rat pups exposed to valproic acid (VPA) (600 mg/kg, intraperitoneally) wereexamined on postnatal day 48–50 (PND 48–50) using marble-burying task (MBT), open field, novel object recognition (NOR), and Passive avoidance tasks. Famotidine (FAM) (10, 20, and 40 mg/kg, intraperitoneally) was also used to determine whether histaminergic neurotransmission exerts its procognitive effects via H2 receptors (H2Rs). Furthermore, a histological investigation was conducted to assess the degree of degeneration of hippocampal neurons. The results revealed that repetitive behaviors increased in VPA-exposed rat offspring in the MBT. In addition, VPA-exposed rat offspring exhibited more anxiety-like behaviors in the open field than saline-treated rats. It was found that VPA-exposed rat offspring showed memory deficits in NOR and Passive avoidance tasks. Our results indicated that 3 mg/kg CPX improved cognitive impairments induced by VPA, while 20 mg/kg FAM attenuated them. We concluded that 3 mg/kg CPX improved VPA-induced cognitive impairments through H3Rs. The histological assessment showed that the number of CA1 neurons decreased in the VPA-exposed rat offspring compared to the saline-exposed rat offspring, but this decrease was not significant. The histological assessment also revealed no significant differences in CA1 neurons in VPA-exposed rat offspring compared to saline-exposed rat offspring. However, CPX3 increased the number of CA1 neurons in the VPA + CPX3 group compared to the VPA + Saline group, but this increase was not significant. This study showed that rats prenatally exposed to VPA exhibit cognitive impairments in the MBT, open field, NOR, and Passive avoidance tests, which are ameliorated by CPX treatment on PND 48–50. In addition, morphological investigations showed that VPA treatment did not lead to neuronal degeneration in the CA1 subfield of the hippocampus in rat pups.

SUMMARY:Gestational diabetes mellitus (GDM) is one form of diabetes affect approximately 7 % of pregnancies. Diabetic peripheral neuropathy (DPN) is a common complication of diabetes that is associated with loss of nerve fibers, myelin abnormalities and significant decrease in the expression of myelin basic protein (MBP) in peripheral nerves. This study was done to determine the effect of induced diabetes during pregnancy on sciatic nerve in adult rat offspring. In this study, wistar rats' dams were allocated to control and diabetic groups. Diabetic rats were received 40 mg/kg/body weight of streptozotocin (STZ) on the first day of gestation. Six offspring of each group were randomly selected on 12 weeks postnatal and histopathological changes in their nerve tissue were examined through H&E staining and transmission electron microscopy. Furthermore, the expression of MBP in sciatic nerve was examined by immunohistochemistry. We found that the myelinated fiber number of sciatic nerve in offspring of diabetic rats was reduced compared to the controls, but this difference was not significant. The average thickness of the myelin sheath of sciatic nerve fibers in the control and GDM was 97.1±0.1and 94.1±0.2 µm, respectively that the difference was not statistically significant. The expression of MBP protein in the myelin sheath of both groups was similar. TEM results showed that myelin sheath of diabetic offspring had not any changes compared to control. Atrophy of axons and schwannocytus (Schwann cells) alterations were not observed in diabetic offspring. Induction of diabetes during pregnancy reduced the number of nerve fibers and thickness of the myelin sheath. But it has no effect on MBP expression and schwannocytus morphology.