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Oxygen Free Radicals and Endotoxic Shock: Effect of Flaxseed

Toxicology Group, University of Saskatchewan

Kailash Prasad

Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada

Background: Cardiac dysfunction and tissue injury during endotoxemia may be caused by increased levels of oxygen free radicals.

Methods and Results: We therefore investigated the effects of endotoxic shock on cardiac function and contractility, plasma creatine kinase (CK) activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL) and white blood corpuscles, antioxidant reserve (cardiac chemiluminescence [LV-CL]), antioxidant enzyme activity (superoxide dismutase, catalase, glutathione peroxidase), cardiac malondi aldehyde (MDA) concentration, a lipid peroxidation product, and hemodynamics in the absence or prescnce of flaxseed treatment in anesthetized dogs. Flaxseed contains lignans that have antioxidant activities and inhibit platelet-activating factor (PAF). The dogs were assigned to three groups: group I, sham control; group II, endotoxin (ET) treated (5 mg/kg intravenously); group III, ET + flaxseed (2 gm/kg/day orally) for 6 days. ET produced a decrease in cardiac function and contractility and antioxidant enzyme levels, and an increase in cardiac MDA and LV-CL, PMNL-CL, and plasma CK and lactate. Pretreatment with flaxseed attenuated the ET-induced cardiac dysfunction and cellular damage. Protec tion was incomplete for cardiovascular function, plasma CK, and lactate.

Conclusions: These results suggest that oxyradicals and/or PAF may be involved in the deterioration of cardiovascular function and cellular integrity during ET shock and that antioxidant and anti-PAF agents may be effective in the treatment of ET shock.

Key Words: endotoxic shock • oxygen free radicals • cardiovascular function • cellular injury • malondialdehyde • antioxidant reserve • antioxidant enzymes • flaxseed • polymorphonuclear leukocyte chemiluminescence.

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 3, No. 4, 305-318 (1998)
DOI: 10.1177/107424849800300406


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