Effects of Flaxseed Oil on Lead Acetate-Induced Neurotoxicity in Rats
Effects of Flaxseed Oil on Lead Acetate-Induced Neurotoxicity in Rats
Year: 2011
Authors: Abdel Moneim, A.E. Al-Quraishy, S.
Publication Name: Biol. Trace Elem. Res.
Publication Details: DOI 10.1007/s12011-011-9055-4
Abstract:
It is well known that chronic exposure to lead (Pb+2) alters a variety of behavioral tasks in rats and mice. Here, we investigated the effect of flaxseed oil (1,000 mg/ kg) on lead acetate (20 mg/kg) induced brain oxidative stress and neurotoxicity in rats. The levels of Pb+2, lipid peroxidation, nitric oxide (NO), and reduced glutathione (GSH) and the activity of catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione-S-transferase (GST), and glutathione peroxidase (GPx) were determined in adult male albino rats. The level of Pb+2 was markedly elevated in brain and blood of rats. This leads to enhancement of lipid peroxidation and NO production in brain with concomitant reduction in GSH, CAT, SOD, GR, GST, and GPx activities. These findings were associated with DNA fragmentation. In addition, lead acetate induced brain injury as indicated by histopathological changes of the brain. Treatment of rats with flaxseed oil resulted in marked improvement in most of the studied parameters as well as histopathological features. These findings suggest to the conclusion that flaxseed oil significantly decreased the adverse harmful effects of lead acetate exposure on the brain as well as Pb+2 induced oxidative stress. (Authors abstract)
Lead (Pb+2) toxicity remains a significant public health problem because of its global pervasiveness and its adverse effects on the nervous system. Studies suggest that one of the important mechanisms associated with toxic effects of Pb+2 is oxidative stress caused by disrupted prooxidant/antioxidant balance in animals including humans. Reduced glutathione (GSH) levels and glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities in tissues or in blood are most commonly used to evaluate Pb+2-induced oxidative damage. The oxidative stress has also been implicated to contribute to Pb+2-associated tissue injury in the brain, liver, kidneys and other organs. Flaxseed is increasingly used as an ingredient in food because of its high alpha linolenic acid (ALA). The brain is a lipid-rich organ; phospholipids compose nearly 25% of the dry weight of the brain. n3 fatty acids participate in numerous cellular functions, including membrane fluidity, membrane enzyme activities, and eicosanoid synthesis which are essential for brain development in infants and is also required for maintaining normal brain function. This study focuses on the protective role of flaxseed oil against lead acetate-induced neurotoxicity. In this study, induction of lipid peroxidation and increased generation of oxygen-free radicals in tissues from different organs of male mice after inhalation with lead acetate for 1 h suggest the induction of Pb+2 cytotoxicity by indirect mechanisms, i.e., the implication of oxidative stress. Pb+2 may promote free-radical initiated processes in tissues. Changes in activity of some redox system enzymes in brain of Pb+2-intoxicated rats were noted. The consequence of the decrease in the level of tissue antioxidants is due to the increased rate of lipid peroxidation and altered calcium and sulfhydryl homeostasis. All those processes may be associated with enhanced level of ROS in a cell followed by the oxidative stress. The authors suggest a higher level of antioxidant reserve in flaxseed oil combined with Pb+2-treated rats as compared to rats of Pb+2-exposed group only could be due to reduced oxidative stress because of antioxidant activity of lignan complex and hence a reduction in the need for induction of antioxidant reserve. However lignans are not lipid soluble and do not appear naturally in oil. Thus, unless the study utilized lignan-enriched flax oil (which was not mentioned in the paper) the authors have come to an erroneous conclusion. Other natural antioxidants in flax oil such as Vitamin E may be responsible for the result noted. (Editors comments)
Lead (Pb+2) toxicity remains a significant public health problem because of its global pervasiveness and its adverse effects on the nervous system. Studies suggest that one of the important mechanisms associated with toxic effects of Pb+2 is oxidative stress caused by disrupted prooxidant/antioxidant balance in animals including humans. Reduced glutathione (GSH) levels and glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities in tissues or in blood are most commonly used to evaluate Pb+2-induced oxidative damage. The oxidative stress has also been implicated to contribute to Pb+2-associated tissue injury in the brain, liver, kidneys and other organs. Flaxseed is increasingly used as an ingredient in food because of its high alpha linolenic acid (ALA). The brain is a lipid-rich organ; phospholipids compose nearly 25% of the dry weight of the brain. n3 fatty acids participate in numerous cellular functions, including membrane fluidity, membrane enzyme activities, and eicosanoid synthesis which are essential for brain development in infants and is also required for maintaining normal brain function. This study focuses on the protective role of flaxseed oil against lead acetate-induced neurotoxicity. In this study, induction of lipid peroxidation and increased generation of oxygen-free radicals in tissues from different organs of male mice after inhalation with lead acetate for 1 h suggest the induction of Pb+2 cytotoxicity by indirect mechanisms, i.e., the implication of oxidative stress. Pb+2 may promote free-radical initiated processes in tissues. Changes in activity of some redox system enzymes in brain of Pb+2-intoxicated rats were noted. The consequence of the decrease in the level of tissue antioxidants is due to the increased rate of lipid peroxidation and altered calcium and sulfhydryl homeostasis. All those processes may be associated with enhanced level of ROS in a cell followed by the oxidative stress. The authors suggest a higher level of antioxidant reserve in flaxseed oil combined with Pb+2-treated rats as compared to rats of Pb+2-exposed group only could be due to reduced oxidative stress because of antioxidant activity of lignan complex and hence a reduction in the need for induction of antioxidant reserve. However lignans are not lipid soluble and do not appear naturally in oil. Thus, unless the study utilized lignan-enriched flax oil (which was not mentioned in the paper) the authors have come to an erroneous conclusion. Other natural antioxidants in flax oil such as Vitamin E may be responsible for the result noted. (Editors comments)
