The current study aimed to evaluate the harmful effect of chlorpyrifos (CPF) on the reproductive functions and fertility in male rats and to assess the protective role of zinc (Zn) in improving the adverse effects of CPF on male fertility. Sixty mature male rats were divided into four groups: Group 1: The control group was orally administered with the corresponding dose of corn oil. Group 2 animals received chlorpyrifos (1 mg/kg, oral). Group 3 rats received oral zinc (25 mg/kg) daily. Group 4 animals received oral zinc treatment (25 mg/kg). CPF caused a significant decrease in the body and reproductive organs' weights, sperm count, sperm motility percent, serum testosterone, FSH, and LH. The CPF-treated group showed a significant increase in dead sperm percent and sperm abnormalities. CPF induced a significant internucleosomal DNA fragmentation and marked histological alterations in the testes of treated male rats. Conversely, co-treatment with Zn improved the reproductive organs weights, sperm characteristics, internucleosomal DNA fragmentation, and histological alterations of the testes. In conclusion, CPF triggered significant detrimental effects on male reproductive organs and functions and the co-treatment with zinc partly alleviate the injurious effects of CPF on male fertility.

Thiacloprid (TH) is a neurotoxic agricultural insecticide and potential food contaminant. The purpose of this study was to investigate the relationship between TH exposure and memory dysfunction in rats, as well as the potential protective effect of piracetam and piracetam-loaded magnetic chitosan nanoparticles (PMC NPs). Rats were divided into five equal groups (six rats/group). The control group received saline. Group II was treated with PMC NPs at a dose level of 200 mg/kg body weight (Bwt); Group III was treated with 1/10 LD50 of TH (65 mg/kg Bwt); Group IV was treated with TH (65 mg/kg Bwt) and piracetam (200 mg/kg Bwt); Group V was co-treated with TH (65 mg/kg Bwt) and PMC NPs (200 mg/kg Bwt). All animal groups were dosed daily for 6 weeks by oral gavage. Footprint analysis, hanging wire test, open field test, and Y-maze test were employed to assess behavioral deficits. Animals were euthanized, and brain tissues were analyzed for oxidative stress biomarkers, proinflammatory cytokines, and gene expression levels of glial fibrillary acidic protein (GFAP), amyloid-beta precursor protein (APP), B-cell lymphoma 2 (Bcl-2), and caspase-3. Brain and sciatic nerve tissues were used for the evaluation of histopathological changes and immunohistochemical expression of tau protein and nuclear factor kappa B (NF-κB), respectively. The results revealed that TH-treated rats suffered from oxidative damage and inflammatory effect on the central and peripheral nerves. The administration of PMC NPs considerably protected against TH-induced neuronal damage, increased antioxidant enzyme activity, decreased inflammatory markers, and improved behavioral performance than the group treated with piracetam. The neuroprotective effect of PMC NPs was mediated through the inhibition of GFAP, APP, caspase-3, Tau, and NF-κB gene expression with induction of Bcl-2 expression. In conclusion, TH could induce oxidative stress, inflammatory and neurobehavior impairment in rats. However, PMC NPs administration markedly mitigated TH-induced brain toxicity, possibly via oxidative and inflammatory modulation rather than using piracetam alone.

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