This experiment was performed to evaluate the possible embryotoxic and teratogenic effects of doxycycline during rat development. Twenty‐one female rats were used and distributed into three groups equally (seven animals/group). The low dose group received doxycycline at a dose of 5 mg/kg bw/day orally from the 6th to 14th day of gestation. The high dose group received 10 mg/kg bw/day orally for the same period, the Control group received 1 mL distilled water orally for the same period. The dams were dissected on the 20th day of gestation and their fetuses were subjected to morphological, skeletal, and histological examination. Moreover, DNA damage analysis of liver cells of pregnant rats and their fetuses or fetal skull was assessed by Comet assay. The obtained results showed a significant decrease in fetal body weight, several morphological anomalies, and severe lack of ossification on the skull bones, phalanges, and sternum bone as well as shortness in the ulna and radius bones. Histological studies of pregnant rats revealed congestion and dilatation of the central vein of the liver lobules and fatty degeneration of the hepatocytes. In addition, 20 day‐fetuses showed a marked increase of necrotic hepatocytes associated with an increased average of megakaryocytes and periportal leukocytic infiltration. Moreover, doxycycline induced a significant increase in the percentage of DNA damage and tail length of examined samples. Conclusively, doxycycline caused certain fetal abnormalities, so it is advisable to avoid using this drug during pregnancy.

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Neonicotinoid insecticides usage is currently widespread, but this poses a challenge when considering the potential for occupational and environmental contamination. One of the most extensively used insecticides is thiamethoxam (TMX), a second-generation neonicotinoid insecticide. This study aimed to see if sub-lethal dosages of TMX insecticide had any negative impacts on epididymal sperm parameters, serum hormones, oxidative status, and testicular histology. The experimental cohorts were given a low dose of TMX (156 mg/kg bw), a high dose of TMX (312 mg/kg bw), or an untreated control for eight weeks. The sperm count, percent of viability, motility, and motility progressing and fructose level significantly decreased in both TMX-treated groups compared to the control group. Furthermore, TMX administration induced sperm morphological defects, serum hormone disturbances as significant reduction testosterone level, oxidant/antioxidant status imbalance as significant decline in catalase (CAT) and glutagthione peroxidase (GSH) content and significant rise in malondialdehyde (MDA) level and testicular histopathological alternation. TMX caused significant increase DNA damage in testicular tissue represented in tail DNA percent, comet percent, comet length, tail moment, and Olive moment. In conclusion, TMX exposure may have a deleterious impact on male albino rats' fertility through spermatogenesis, steroidogenesis and testicular redox status disruption, and testicles DNA impairment.

One of the disinfection byproducts of chlorinating drinking water is chloroacetonitrile (CAN). Thirty-six female rats were used and distributed equally into four groups. The low dose treated group received CAN at a dose of 5.5 mg/kg body weight/day (1/40 LD 50 ) orally from the 6th to 12th day of gestation. The high dose treated group received 11 mg/kg body weight/day (1/20 LD 50 ) of CAN orally for the same period, the vehicle control group received 1 mL of corn oil, and the water control group received 1 mL of distilled water orally for the same period. High dose exposure to CAN significantly reduced gravid uterine weight, fetal body weights, and length, and caused obvious skeletal deformities, weak mineralization. Fetal tibial growth plates displayed histopathologic changes. Induced oxidative stress and redox imbalance in fetal liver tissues was evidenced by significantly decreased in catalase and superoxide dismutase activity, and elevated malondialdehyde levels. Histopathological, glycogen content changes, and DNA damage were observed in the fetal liver of high dose treated group. Additionally, administration of high dose of CAN induced apoptosis, evidenced by increased caspase-3 concentration in fetal liver. Thus, extensive exposure to CAN induces poor pregnancy outcomes.CAN levels in water should be monitored regularly. K E Y W O R D S chloroacetonitrile, DNA damage, fetal liver, rat, water disinfection byproducts Highlights • Pregnant rats were given chloroacetonitrile (CAN) orally during organogenesis. • Extensive exposure to CAN caused a reduction in lengths of fetal bones and damage to fetal hepatic tissues. • High dose maternally treated fetuses showed elevated levels of caspase-3 activity and DNA damage.

In the current study, we synthesized and prepared a curcumin and vitamin E nanocomposite coated with olive oil (CEONC). Curcumin, vitamin E, and olive oil are fundamental organic antioxidants, and forming nanoparticles from these components endows them with special characteristics. We investigated the protective effect of CEONC on reproductive toxicity induced by cadmium chloride (CdCl2) in male rats. Forty rats (170–180 g) were randomly assigned to four groups: Group 1 (control) received oral distilled water; Group 2 intraperitoneal injection with CEONC (30 mg/kg); Group 3 received oral CdCl2 (5 mg/kg); and Group 4 received CdCl2 (5 mg/kg) followed by CEONC (30 mg/kg) for 4 weeks. After 50 days, we terminated the experiment and assessed male reproductive hormones, sperm motility, viability and morphology, and testes histopathology and conducted a comet assay. The results revealed that co‐administration of CEONC with CdCl2 exposure increased reproductive hormone levels, improved sperm motility and viability, prevented sperm morphological changes, recovered the testicular histology, and decreased DNA damage in the testicular tissue compared to rats exposed to CdCl2 alone. CEONC administration produced no adverse effects and enhanced all sperm parameters. Our findings demonstrate that CEONC is a potential treatment for preventing reproductive damage induced by cadmium exposure.