Introduction:Antibiotic abuse is a common phenomenon in Egypt as medications are prescribed without supervision. It is suggested that the excess use of antibiotics modifies the gut microbiota and plays a role in the development of neurological and psychiatric disorders.Objective:The aim of the present study was to use bulb-c mice as models for curam (amoxicillin /clavulanic acid) abuse compared to the locally acting neomycin model, then restoring the probiotic balance to look at the possible effects on the animal brains.Methods:The results showed early excitable brains demonstrated by S100b immunohistochemistry in both cortexes and hippocampuses of neomycin-treated mice. Staining with PAS stain showed no suggested neurodegenerative changes. Treatment with probiotics improved the S100b immunohistochemistry profile of the curam group partially but failed to overcome the neuroinflammatory reaction detected by hematoxylin and eosin stain. Curam was possibly blamed for the systemic effects.Results:The neurobehavioral tests showed delayed impairment in the open field test for the curam group and impaired new object recognition for the neomycin group. These tests were applied by video recording. The neurobehavioral decline developed 14 days after the end of the 3-week antibiotic course. Unfortunately, curam abuse induced animal fatalities.Conclusion:Antibiotic abuse has a neurotoxic effect that works by both local and more prominent systemic mechanisms. It can be said that antibiotic abuse is a cofactor behind the rise of neuropsychiatric diseases in Egypt.

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Rotenone is widely used insecticide and pesticide. It is an environmental neurotoxin that induces accumulation of α-synuclein and deterioration of dopaminergic neurons in substantia nigra pars compacta (SNpc). Autophagymediated self-digestion of cytoplasmic inclusions may be defensive against neurodegeneration caused by rotenone toxicity. This study designed to assess the autophagy role in rotenone-induced neurotoxic effects. Sixteen C57 black 6 male mice were divided into rotenone & control groups, each group contains 8 mice: the rotenone group; mice were administrated rotenone (3 mg/kg/day intraperitoneally). In the control group carboxymethyl cellulose 0.5% (a vehicle for rotenone) was given as 3mL/Kg/day intraperitoneal. Neuro-behavioural locomotor tests, histopathological and immuno-histochemical analysis of the brain dopaminergic neuronal cells and counting of microtubule Associated Protein Light Chain 3 (LC3) positive cells expression were investigated. Results showed that rotenone administration increases the total distance travelled, numbers of line crossing, average speed, maximum speed and rotations of the animal's body. However, it significantly decreases the efficient path and the total mobile and immobile episodes and induced severe degenerative changes in histo-pathological examination. Also, it decreased significantly the quantity of LC3 positive cells in the brain sections of exposed mice i.e. neurodegeneration and inhibition of autophagy in dopaminergic system. From this study it can be concluded that rotenone can induce neurotoxicity through inhibition of autophagy.

Bisphenol-A (BPA) is one of the commonest chemicals used in the manufacturing of plastics. Childhood obesity is one of the most serious public health challenges of the 21 st century that affects many low-and middle-income countries, including Egypt. This study was conducted to correlate between BPA exposure and risk of obesity in a sample of Egyptian children and to find out whether adiponectin (ADP) can be utilized as an exposure biomarker or not. This study was conducted on 80 children. They were divided into two groups according to their body mass index (BMI): Study group included 40 obese children (BMI ≥ 95 th percentile), and control group included 40 normal-weight children (BMI 5 th-85 th percentile). Levels of urinary BPA and serum ADP were estimated using HPLC and ELISA respectively. The study revealed that statistically significant increase in mean adjusted urinary BPA levels (P < 0.001) and serum ADP levels (P < 0.001) between study and control groups. Within the study group, a statistically significant positive correlation was found between urinary BPA levels and BMI (r = 0.956), meanwhile, statistically significant negative correlations were found between urinary BPA levels and serum ADP levels, as well, serum ADP levels and BMI (r=-0.947,-0.984 respectively). Binary logistic regression analysis showed that odds ratio for serum ADP level was 0.146 with 95% CI: 0.003-0.66, P=0.012. Significant increased risk for obesity among BPA exposed children was found and ADP can be used as a predictor biological marker for BPA-induced obesity.