title: Amelioration of the cardiovascular manifestations of the yellow scorpion Leiurus quinquestriatus envenomation in rats by red grape seeds proanthocyanidins.
abstract: The study attempts to determine the involvement of oxidative stress in cardiovascular manifestations during Leiurus quinquestriatus quinquestriatus (LQQ) scorpion envenomation and to examine the possible protective role of red grape seed proanthocyanidins (GSP) against such effects. Lethality studies conducted in mice demonstrated a significant (p<0.01) protection of GSP against venom lethality. Pretreatment with GSP (200 mg kg(-1), p.o., 10 days) prior to venom injection (350 microg kg(-1), s.c.) resulted in a significant decrease in percent mortality as well as in significant prolongation of the animal's survival time (p<0.01). Monitoring the cardiovascular effects elicited by venom injection in anesthetized rats revealed a marked protection of GSP against the increase in mean arterial blood pressure evoked by LQQ venom. Moreover, pretreatment with GSP reduced the characteristic signs of conduction defects, myocardial ischemia, and infarction observed by venom injection. Biochemical analyses showed that scorpion envenomation caused significant (p<0.001) elevation in serum lactate dehydrogenase as well as creatine kinase-MB activities. Such elevation was ameliorated by GSP (p<0.001). Oxidative stress parameters revealed that scorpion venom significantly increased (p<0.001) the level of lipid peroxidative damage in cardiac tissues and reduced the activity of both glutathione reductase and glutathione peroxidase enzymes in cardiac tissues (p<0.05). In the meantime, GSP offered significant protection against lipid peroxidative damage (p<0.05) and enhanced cardiac glutathione reductase activity (p<0.001). In summary, the current study demonstrates that pretreatment with GSP offers significant protection against LQQ envenomation possibly via enhancement of the antioxidant defense systems.
authors.affiliation: Pharmacology Department, School of Pharmacy, University of Mississippi, MS 38677, USA.
authors.forename: Abir T
authors.initials: AT
authors.lastname: El-Alfy
authors.forename: Amany A E
authors.initials: AA
authors.lastname: Ahmed
authors.forename: Amal J
authors.initials: AJ
authors.lastname: Fatani
authors.forename: Farida
authors.initials: F
authors.lastname: Kader
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography / Q000187:drug effects; D005980:Glutathione Reductase / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D009195:Peroxidase / Q000378:metabolism; D044945:Proanthocyanidins / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012604:Scorpion Venoms / Q000633:toxicity*; D012605:Scorpions / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D027843:Vitis / Q000737:chemistry*
chemical_list: D015415:Biomarkers; D044945:Proanthocyanidins; D012604:Scorpion Venoms; D009195:Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase