Abdulrahman Al Asmari

Effects of Echis pyramidum Snake Venom on Hepatic and Renal Antioxidant Enzymes and Lipid Peroxidation in Rats

The effects of Echis pyramidum venom (EPV) (0.25, 0.50, and 1.00 mg/kg) on activities of superoxide dismutase (SOD) and catalase (CAT) and levels of thiobarbituric acid reactive substances (TBARS) and total thiols (T‐SH) in liver and kidneys of rats were investigated. EPV significantly and dose dependently decreased the activities of SOD and CAT in livers. Although the kidney SOD and CAT activities were not affected by low and medium doses of EPV, the high dose significantly reduced the activities of these enzymes. Liver and kidney TBARS levels were not affected by the low and medium doses of EPV, whereas the high dose significantly increased the TBARS after 6 h postdosing. There was a significant depletion of T‐SH in liver and kidneys of rats exposed to a high dose of EPV. The acute phase oxidative stress due to an EPV injection points toward the importance of an early antioxidant therapy for the management of snake bites.

Vanillin abrogates ethanol induced gastric injury in rats via modulation of gastric secretion, oxidative stress and inflammation

Vanillin is commonly used as an additive in food, medicine and cosmetics, but its effect has not yet been studied in gastric injury. Therefore the effect of vanillin was studied in experimental gastric ulcer. Gastric secretion and acidity were studied in pylorus ligated rats. Ulcer index, levels of gastric mucus, malondialdehyde (MDA), myeloperoxidase activity (MPO), expression of nuclear factor kappa B (NF-κB) p65, and histopathological changes were determined in ethanol induced gastric ulcer. Pre treatment with vanillin significantly reduced gastric secretion (P < 0.001) and acidity (P < 0.0001) and gastric ulcer index scores (P < 0.001). and augmented the gastric mucosal defense. Vanillin significantly restored the depleted gastric wall mucus levels (P < 0.0001) induced by ethanol and also significantly attenuated ethanol induced inflammation and oxidative stress by the suppression of gastric MPO activity (P < 0.001), reducing the expression of NF-κB p65 and the increased MDA levels (P < 0.001). Vanillin was also effective in alleviating the damage to the histological architecture and the activation of mast cells induced by ethanol. Together the results of this study highlight the gastroprotective activity of vanillin in gastric ulcers of rats through multiple actions that include inhibition of gastric secretion and acidity, reduction of inflammation and oxidative stress, suppression of expression of NF-κB, and restoration of the histological architecture.

The Role of Apolipoprotein E Gene Polymorphisms in Primary Glaucoma and Pseudoexfoliation Syndrome

Primary glaucoma (PG) is one of the most common eye diseases which may potentially result in bilateral blindness. Glaucoma affects 70 million people and is the second leading cause of blindness worldwide. It is estimated that by the year 2020, this number would rise to around 79.6 million [1]. The prevalence of glaucoma varies widely across the different ethnic groups [2-8] and is significantly higher in blacks (4.7%) as compared to the white (1.3%) population [9]. The prevalence of both primary open angle glaucoma (POAG) and primary angle closure glaucoma (PACG) is higher in western region of Saudi Arabia as compared to other Asian countries [10]. To date no national study has been undertaken to determine the exact preva‐ lence of glaucoma in Saudi Arabia, though it is one of the major causes of blindness in this country.

Identification and phylogeny of Arabian snakes: Comparison of venom chromatographic profiles versus 16S rRNA gene sequences.

Identification of snake species is important for various reasons including the emergency treatment of snake bite victims. We present a simple method for identification of six snake species using the gel filtration chromatographic profiles of their venoms. The venoms of Echis coloratus, Echis pyramidum, Cerastes gasperettii, Bitis arietans, Naja arabica, and Walterinnesia aegyptia were milked, lyophilized, diluted and centrifuged to separate the mucus from the venom. The clear supernatants were filtered and chromatographed on fast protein liquid chromatography (FPLC). We obtained the 16S rRNA gene sequences of the above species and performed phylogenetic analysis using the neighbor-joining method. The chromatograms of venoms from different snake species showed peculiar patterns based on the number and location of peaks. The dendrograms generated from similarity matrix based on the presence/absence of particular chromatographic peaks clearly differentiated Elapids from Viperids. Molecular cladistics using 16S rRNA gene sequences resulted in jumping clades while separating the members of these two families. These findings suggest that chromatographic profiles of snake venoms may provide a simple and reproducible chemical fingerprinting method for quick identification of snake species. However, the validation of this methodology requires further studies on large number of specimens from within and across species.

An Overview of Target Specific Neuro-Protective and Neuro-Restorative Strategies

The cellular mechanisms underlying neuronal loss and neurodegeneration have been an area of great interest for neuroscientists throughout the world. The development of animal models that simulate critical components of clinical neurodegenerative diseases have provided tremendous insight into the pathophysiological pathways and have facilitated the application of targeted pharmacotherapy. Although neurodegenerative diseases (ND), such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), and multiple sclerosis (MS) each have distinct clinical symptoms and pathologies, they also share common mechanisms such as intraand/or extracellular accumulation of misfolded proteins; apoptosis; neuroinflammation; mitochondrial injury, oxidative stress and excitotoxic insult (Tarawneh and Galvin, 2010). No one mechanism appears to be primary in all cases of a particular ND, and these pathogenic most mechanisms most likely act synergistically through complex interactions to promote neurodegeneration. Discussion of these mechanisms is briefly reviewed here in reference to their implications for the development of novel neuroprotective /neuro-restorative agents targeting one or more of these pathways.