الفهرس 
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Abstract
Di (2-ethylhexyl) phthalate (DEHP) and bisphenol A are the most common plasticizers that are used to manufacture polyvinyl chloride and polycarbonate plastics, respectively. Several studies demonstrated the neurobehavioral toxic effects induced by DEHP and BPA. Study 1: We investigated the neurotoxic effects of various dosages of DEHP on male rats, including 50,300,750 mg/kg bw orally for 28 days. Our finding revealed that three doses of DEHP induce spatial working memory impairment. Furthermore, 300 and 750 mg/kg doses produce anxiety-like behavior and deficiencies in recognition memory. However, all toxicity groups exhibited a significant increase in brain pro-inflammatory associated with the triggering production of TLR4-NF-kβ as well as an increase in brain level of NPY and caspase-3; the neurotoxicity was confirmed by disruption of brain architecture. Moreover, the nutraceutical compounds have been confirmed as potent antioxidants and anti-inflammatories in neurotoxicity. Thus, in study 2, we examine the therapeutic effects of ferulic acid (FA) in male rats exposed to DEHP. Four groups of male rats were established, with group 1 receiving corn oil, group 2 receiving 300 mg/kg of DEHP, group 3 receiving 50 mg/kg of FA plus 300 mg/kg of DEHP, and group 4 receiving 50 mg/kg of FA orally for 30 days. Our results indicated that FA could ameliorate anxiety-like behavior as well as deficiencies in working and long-term memory induced by DEHP. Moreover, FA alleviates brain oxidative stress biomarkers, BDNF, and brain HO-1 levels, in conjunction with mitigating the degeneration of different brain regions and immunohistochemistry of caspase-3 levels. Besides, in study 3, FA was evaluated against BPA-induced Alzheimer’s disease-like pathology. Males Wistar were randomly assigned into the following four groups: Corn oil, BPA 50 mg/kg, BPA 50 mg/kg + FA 50 mg/kg, and FA 50 mg per os for 40 days. We observed that FA could mitigate Alzheimer’s disease-like changes induced by BPA as FA improves spatial working memory and recognition memory in male rats. FA has also improved the levels of brain oxidative stress biomarkers, inflammatoy, and apoptotic indicators. In addition, the amyloid protein and Tau protein expression levels were significantly reduced in the BPA 50 mg/kg plus FA 50 mg/kg group. These neuroprotective improvements were confirmed by restoring brain architecture and a considerable decrease in GFAP expression produced by FA therapy. In study 4, we investigate the neurocognitive toxic effects of DEHP on different generations, including F1 and F2 generations, as well as the paternal effect of DEHP on male pups. Male pups from both generations were tested, such as F1. PD, F2. PDF, F2. PF, and F2. PD compared to control pups. Our results revealed that second-generation male pups, including F2. PDF and F2. PD displayed anxiety-like behavior compared to the first generation. On the contrary, all intoxicated male pups from the first and second generations displayed significant spatial working memory and long-term memory impairment compared to control pups. Furthermore, groups of F2. PDF and F2. PD showed severe destructive changes in CA3, cerebral cortex, associated with a marked increase in brain apoptosis compared to other groups. In conclusion, DEHP and BPA induce neurotoxic effects in male rats, which FA may ameliorate. Further, DEHP’s neurotoxicity is multigenerational and has a substantial paternal influence on male offspring.