Protective Role of Ellagic Acid Against Ethanol-Induced Neurodevelopmental Disorders in Newborn Male Rats: Insights into Maintenance of Mitochondrial Function and Inhibition of Oxidative Stress.

OBJECTIVE: Ellagic acid (EA) exerts, neuroprotective, mitoprotective, anti-oxidative and anti-inflammatory effects. We evaluated protective effect of EA on ethanol-induced fetal alcohol spectrum disorders (FASD). METHODS: A total of 35 newborn male rats were used, divided into five groups, including; control (normal saline), ethanol (5.25 g/kg per day), ethanol (5.25 g/kg per day) + EA (10 mg/kg), ethanol (5.25 g/kg per day) + EA (20 mg/kg) and ethanol (5.25 g/kg per day) + EA (40 mg/kg). Thirty-six days after birth behavioral tests (Morris water maze and Elevated Plus Maze), tumor necrosis factor-α (TNF-α) levels, oxidative markers (malondialdehyde, glutathione and superoxide dismutase), mitochondrial examination such as succinate dehydrogenases (SDH) activity, mitochondrial swelling, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) formation were analyzed. RESULTS: The results revealed that ethanol exposure adversely affected cognitive and mitochondrial functions and as well as induced oxidative stress and inflammation in brain tissue. However, EA (20 and 40 mg/kg) administration effectively prevented the toxic effects of ethanol in FASD model. CONCLUSIONS: These findings demonstrate that ethanol application significantly impairs the brain development via mitochondrial dysfunction and induction of oxidative stress. These data indicate that EA might be a useful compound for prevention of alcohol-induced FASD.

Hydrogen sulfide improves spatial memory impairment via increases of BDNF expression and hippocampal neurogenesis following early postnatal alcohol exposure.

According to experimental and clinical findings, fetal brain development may be interrupted by maternal alcohol consumption during pregnancy. Adult hippocampal neurogenesis is thought to play a role in cognition function (i.e. learning and memory). Recent evidence suggests that ethanol administration causes major apoptotic neurodegeneration in many regions of the rats' developing brain during the synaptogenesis period. Based on the recent studies, H2S improve learning and memory via increased neurogenesis and antiapoptotic mechanisms in different animal models. In this study, we aimed to evaluate the protective effects of hydrogen sulfide on alcohol-induced memory impairment, hippocampus neurogenesis and neuronal apoptosis in rat pups with postnatal ethanol exposure. Administration of ethanol to male rat pups was performed through intragastric intubation on postnatal days 2-10. The pups were administered 1 mg/kg of NaHS (H2S donor) on postnatal days 2-10. For examining the spatial memory, Morris water maze test was carried out 36 days after birth. Following the behavioral test, immunohistochemical staining was performed to evaluate the expression levels of BrdU, BDNF and Apoptotic cell death was detected by TUNEL staining. Hydrogen sulfide (H2S) treatment could significantly improve spatial memory impairment (P < 0.05) and significantly increase the expression of BrdU and BDNF in dentate gyrus area (P < 0.05). It also decreased positive TUNEL cells, compared with the ethanol group (P < 0.01). Based on the findings, H2S makes significant neuroprotective effects on Ethanol neurotoxicity due to its neurogenesis and anti-apoptotic activity.

Sulfur dioxide reduces hippocampal cell death and improves learning and memory deficits in a rat model of transient global ischemia/reperfusion.

OBJECTIVES: According to recent the findings, sulfur dioxide (SO2) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO2 exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objective of the current study was to examine the neuroprotective impact of SO2 following global cerebral ischemia/reperfusion (I/R). MATERIALS AND METHODS: Forty-eight male Wistar rats that weighed 260-300 g, were randomly allocated into 4 groups: sham group (n=12), I/R group (n=12), and I/R+SO2 groups (NaHSO3 and Na2SO3; 1:3 ratio; 5 and 10 µg/kg, respectively; for 3 days, n=12). Cerebral ischemia model was prepared by occlusion of both common carotid arteries for 20 min. Saline as a vehicle and SO2 donor at doses 5 µg/kg (intraperitoneally) were injected for 3 days after reperfusion. Four days after ischemia, the passive avoidance memory test was carried out in four groups, and after behavioral assessment, necrosis, apoptosis, and antioxidant enzyme analysis were carried out. RESULTS: O2 treatment could significantly improve memory impairments in rats with cerebral ischemia/reperfusion (I/R) (P<0.05). An increase in both superoxide dismutase and glutathione and a reduction in malondialdehyde were reported in the SO2 group versus the ischemic group (P<0.05). Moreover, SO2 could significantly decrease necrotic and apoptotic cells in the CA1 region (P<0.01). CONCLUSION: According to the findings, SO2 exerts significant neuroprotective effects on cerebral I/R due to its antioxidant activity.

Microbiological qualification of air, water and dialysate in a haemodialysis centre: a new focus on Legionella spp.

BACKGROUND AND OBJECTIVES: The microbiological monitoring of the water used for haemodialysis is important especially for Legionella and non-fermentative bacteria since patients with end stage renal disease (ESRD) are suffering from deteriorated function of immune system. MATERIALS AND METHODS: A total 50 water and dialysate samples were weekly collected over a period of 10 weeks from 5 sites. Total and faecal coliforms were determined by utilizing the most probable number (MPN) method. For isolation of Legionella, water samples were inoculated on a BCYE medium. DNA extraction was performed and was used to amplify 16S rRNA gene of Legionella species. Airborne bacteria were sampled using a single stage Andersen air sampler. RESULTS: Out of total 50 water samples, 24 samples had bacterial contamination. The highest rate of Legionella contamination was observed in the storage tank (67 cfu/ml). Legionella was not isolated from the dialysate effluent samples. The highest rate of total bacterial count was related to the dialysate effluent and the maximum total count of coliforms was related to the reverse osmosis. The isolated bacteria were Gram-negative bacilli (mostly Pseudomonas isolates), Gram-positive cocci (mostly Micrococcus spp.) and Gram-positive bacilli (mostly Bacillus spp.). Six samples were contaminated with coliforms. No faecal coliform was isolated from the samples. CONCLUSION: These results indicated that dialysis machine is an important source of contaminations such as Staphylococcus, Pseudomonas and Legionella. Therefore an efficient prevention program is needed to eliminate bacterial contamination of dialysis water system. Moreover, in haemodialysis centres, periodic surveillance programs for microbiological qualification can lead to a better planning for disinfection of haemodialysis water systems.