Lead-induced Lipid Peroxidation Research Articles

Inhibitory effect of Solanum anguivi fruit extracts against lead-induced lipid peroxidation in rat liver and kidney

Rapid incidence of liver and kidney disorders resulting in high mortality nowadays is of great concern and there is this very need to salvage the sudden death resulting from the disorders. Lipid peroxidation which is the hallmark of oxidative stress that damage body tissues is prominent as one of the causative factors leading to many chronic and degenerative diseases. This study is sought to investigate the inhibitory effect of aqueous and ethanolic extracts of Solanum Anguivi fruit against lead acetate induced lipid peroxidation in the liver and kidney tissues of albino rats in vitro using thiobarbituric acid reactive substances (TBARS) assay. The results obtained indicate a concentration dependent increase in inhibitory potential of the extracts against lead acetate in both liver and kidney tissues. Highest extract inhibitory potential was (90%) at highest extract concentration (160mg/ml) and this was obtained in the liver tissue. Hence, the results from this study suggest that oxidative stress in liver and kidney tissues could be potentially prevented or managed by dietary intake of Solanum Anguivi fruits.

Therapeutic Efficiency of spirulina against Lead Acetate Toxicity on the Fresh Water Fish Labeo rohita

The release of heavy metals in to the aquatic environment causes water pollution problems because of their toxicity, persistence and bioaccumulation. Lead has no known role to play in the human body that is physiologically relevant, and its harmful effects are myriad. Lead from the atmosphere and soil ends up in water bodies thus affecting the aquatic organisms. This situation has thus prompted numerous investigators to study on the effects of this heavy metal on the biological functions of aquatic organisms, particularly on the antioxidant enzyme activity in fish. In the present investigation the effect of lead acetate (heavy metal) on antioxidant enzyme activity was evaluated in the fresh water fish Labeo rohita. The experimental fish were treated with sub lethal concentration of lead acetate (0.015 mg/ L) for 120 hrs. Spirulina was used as supplementary feed during the experimental period. We observed various lead induced lipid peroxidation (LPO), antioxidant enzyme (SOD and CAT) changes and Spirulina supplementary feed therapeutic efficiency was observed in the gill and liver tissues of the fish. All the experimental data are statistically significant at p<0.05% level. The present study was under taken the toxic effect of lead acetate on Labeo rohita fish and chelating property of Spirulina.

Antioxidant and micronutrient-rich milk formula reduces lead poisoning and related oxidative damage in lead-exposed mice

Lead poisoning is a global environmental disease that induces lifelong adverse health effects. The effect of a milk formula consisting of antioxidant of bamboo leaves (AOB), vitamin C (Vc), calcium lactate (CaLac), ferrous sulfate (FeSO₄) and zinc sulfate (ZnSO₄) on the reduction of lead and lead-induced oxidative damage in lead-exposed mice was studied. The lead-reducing effect of milk formula was investigated via a 7-week toxicokinetics study and a tissue distribution level examination. The ameliorating effect of milk formula on lead-induced oxidative damage was investigated. Results demonstrated current milk formula could effectively reduce blood lead levels (BLLs) and lead distribution levels of liver, kidneys, thighbones and brain in mice based on metal ion-mediated antagonism and chelation mechanisms. This milk formula could not only protect lead-susceptible tissues against lead poisoning, but also maintain normal absorption and distribution of essential elements in vivo. Meanwhile, current milk formula could prevent the reduction of δ-aminolevulinic acid dehydratase (δ-ALAD) activity and enhancement of free erythrocyte protoporphyrins (FEP) levels in blood erythrocytes of mice. Also, this formula could indirectly protect blood cell membranes against lead-induced lipid peroxidation. We conclude that current optimized milk formula effectively reduces lead poisoning and lead-induced in vivo oxidative damage in lead-exposed mice.

The impact of allicin on lead-induced oxidative damage in selected organs of the common carp (Cyprinus carpio)

Lead-induced oxidative stress contributes to the pathogenesis of lead poisoning. Considering the antioxidant properties of allicin, the objective of this study was to evaluate the efficacy of allicin in preventing lead-induced oxidative damage in the liver, kidney, brain, and gill of the common carp. Fish were divided randomly into five groups, depending on the combination of lead acetate and allicin treatments. The oxidative stress was measured by the malondialdehyde (MDA) level, reduced glutathione (GSH) content, and by enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in tissue homogenates. Lead acetate exposure (7.0 mgL−1, 10 days) caused a significant decrease in GSH concentration in the liver, kidney, and brain; SOD activity in the liver, kidney, and gill; and GPx activity in the liver and brain. MDA content in the liver, kidney, brain, and gill showed a significant increase following lead acetate treatment compared with the normal control group. Administration of allicin was markedly effective in decreasing lead-induced lipid peroxidation and increasing the cellular antioxidant enzyme activities and GSH levels. These results suggest that allicin can modulate lead-induced oxidative stress and might have some therapeutic and prophylactic effects on lead poisoning.

Beneficial Effect of Combined Administration of Vitamin C and Vitamin E in Amelioration of Chronic Lead Hepatotoxicity

Introduction: Oxidative stress with subsequent lipid peroxidation has been postulated as one mechanism for lead toxicity. The protective action of vitamins C and E against lead affects lipid hydroperoxide level and liver functions in male rats has been studied. Results: Administration of lead acetate (2%) in dirinking water for 3 months elevates plasma lipid hydroperoxide level, activities of aspartate aminotronsferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), cholesterol, triglycerides and low density lipoprotein (LDL) levels. On the other hand, reduced plasma glutathione (GSH), protein and high density lipoprotein (HDL) concentrations lowered significantly in lead (Pb) treated group. However, oral administration of vitamin C (Vit C) or vitamin E (Vit E) at dose level of 100 mg/kg body weight reduced the alterations in the previous parameters. On the other hand, co-administration of both vitamins (Vit C+ Vit E) to lead-treated rats led to the most significant decline in lipid hydroperoxide level, restoration of GSH level and exhibited more protection as compared with Vit C or Vit E separately. Conclusion: There is synergistic antioxidative effect between Vit C and Vit E that protects the liver from lead induced lipid peroxidation, suggesting that the antioxidant treatment may best be done using a balanced cocktail. .

N-Acetylcysteine Exposure on Lead-Induced Lipid Peroxidative Damage and Oxidative Defense System in Brain Regions of Rats

Lead (Pb) is known to disrupt the pro-oxidant/antioxidant balance of tissues, which leads to biochemical and physiological dysfunction. Oxidative stress is considered a possible molecular mechanism involved in Pb neurotoxicity. Considering the vulnerability of the brain to oxidative stress under Pb neurotoxicity, this study investigated the effects of exposure of the thiol antioxidant N-acetylcysteine (NAC) on lead-induced oxidative damage and lipid peroxidation in brain regions of the rat. Wister strain rats were exposed to lead in the form of lead acetate (20 mg/kg body wt/d) for a period of 2 wk and the effects of NAC on lead-induced neurotoxicity in rat brain regions were assessed by postadministration of NAC (160 mg/kg body wt/d) for a period of 3 wk. The lipid peroxidation byproduct, malondialdehyde (MDA) increased following lead exposure in both of the regions, and the antioxidant capacities of the cell in terms of the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) was diminished. Following NAC treatment, lead-induced lipid peroxidation decreased and antioxidant enzyme activities improved, with CAT showing enhancement in the cerebral region only and SOD showing enhancements in the cerebellar region. Our result suggests that thiol-antioxidant supplementation following Pb exposure might enhance the reductive status of brain regions by arresting the lipid peroxidative damage in brain regions.

Combined efficacies of lipoic acid and 2,3-dimercaptosuccinic acid against lead-induced lipid peroxidation in rat liver

Oxidative stress with subsequent lipid peroxidation has been postulated as one mechanism for lead toxicity. Hence in assessing the protective effects of lipoic acid (LA) and meso 2,3-dimercaptosuccinic acid (DMSA) on lead toxicity, they were tested either separately or in combination for their effects on selected indices of hepatic oxidative stress. Elevated levels of lipid peroxides were accompanied by altered antioxidant defense systems. Lead acetate (Pb - 0.2%) was administered in drinking water for five weeks to induce toxicity. LA (25 mg kg −1 body wt. day −1 i.p) and DMSA (20 mg kg −1 body wt. day −1 i.p) were administered individually and also in combination during the sixth week. Lead damage to the liver was evident in the decreases in hepatic enzymes alanine transaminase (−38%), aspartate transaminase (−42%) and alkaline phosphatase (−43%); increases in lipid peroxidation (+38%); decreases in the antioxidant enzymes catalase (−45%), superoxide dismutase (−40%), glutathione peroxidase (−46%) and decreases in glutathione (−43%) and decreases in glutathione metabolizing enzymes, glutathione reductase (−59%), glucose-6-phosphate dehydrogenase (−27%) and glutathione-S-transferase (−42%). In combination LA and DMSA completely ameliorated the lead induced oxidative damage. Either compound alone was however only partially protective against lead damage.

Lead-induced lipid peroxidation and antioxidant defense components of developing chick embryos

Administration of lead (1.25 and 2.5 μmol/kg egg weight) to 14-day-old chick embryos enhanced the level of lipid peroxides (LPO) in tissues of liver, brain, and heart. Accumulation of LPO was maximum at 9 h after treatment with lead and returned to normal level by 72 h. Further, we have studied the levels of glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx), superoxida dismutase (SOD), and catalase. AT 9 h posttreatment, the hepatic GR was reduced significantly with the induction of GST and considerable depletion of GSH. However, in brain and heart, both GR and GST activities were unaltered with significant reduction of GSH. Further, an increase of non-Se-dependent GPx and SOD activities were observed in liver, brain, and heart. Similarly, at 72 h, although the GPx activity was found decreased in liver and brain, the GST, catalase, and SOD activities were significantly increased in all the three tissues alike, suggesting tissue-specific changes of antioxidant defense components in response to lead treatment. Our results suggest that the elevated levels of GST, SOD, and catalase at 72 h were successful in bringing LPO levels back to normal.