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The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl(3) (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.

No abstract

Noise exposure has been commonly regarded as the main hazard of occupational hearing loss. Recent studies indicate that several chemicals, including organic solvents have ototoxic effects. This study aimed at evaluating the hearing of workers exposed to both noise and a mixture of organic solvents at concentrations anticipated as safe. The study comprised three groups. The first one included 70 workers exposed to noise only, the second group consisted of 93 workers exposed to organic solvents and noise, and the control group included 59 individuals exposed to neither noise nor organic solvents. The three groups were matched for age, socioeconomic status, and smoking habit. The results of this study revealed that there was no statistically significant difference between the two exposed groups as regards the duration of exposure. There was a highly statistically significant difference between the two exposed groups as regards the different types of hearing loss (conductive deafness, sensory neural hearing loss, and mixed type) compared with the control one. Our study reported that sensory neural hearing loss occurred earlier in subjects with combined exposure to noise and solvents at a mean duration of exposure (16.38 ± 9.44 years) compared to (24.53 ± 9.59 years) the subjects with sole exposure to noise. The difference between the two groups was statistically significant regarding this type of hearing impairment (p < 0.05). There was a positive significant correlation between hearing impairment and duration of exposure in the two exposed groups. As regards the results of the environmental monitoring, both noise exposure levels (dB) and levels of different organic solvents measured (mg/m(3)) in different work departments were less than the levels recommended by Egyptian Environmental Law No. 4 for 1994. It is recommended that in the case of combined exposure, noise and solvent levels should be lowered than the permissible limits recommended for either alone.

The role of bisphenol A (BPA) in autism was investigated in 49 children (mean age = 5.950 ± 1.911 years) with autism spectrum disorders (ASDs) and 40 comparable age and sex matched children used as controls (mean age = 5.333 ± 2.279 years). In addition, 8-Hydroxydeoxyguanosine (8-oxodG) was also studied as a biomarker of oxidative stress in the same set of two selected groups. The results showed that both BPA and 8-oxodG were significantly higher in children with autism than those of control children ( values = 0.025 and 0.0001, respectively). There were positive correlations between both BPA and 8-oxodG with ASDs severity ( = 0.400 and 0.805, respectively), these correlations were highly significant ( values = 0.004 and 0.001, respectively). There was a significance positive correlation between BMI and BPA, but the correlation between BMI and 8-oxodG was not significant in children with autism. The observed results revealed that BPA may increase oxidative stress resulting in mitochondrial dysfunction that affecting the behavior and functioning of ASDs children.