الفهرس 
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Abstract
In the present investigation, L-Ascorbic acid, α-tocopherol, and glycine betaine were used to mitigate the harmful effect of lead toxicity. Pb-intoxication was carried out by ingestion of albino rats with 50 mg Pb-acetate/kg body weight daily for 6 weeks. Pb-intoxicated rats were administrated after 4 hours 100mg L-Ascorbic acid /kg body weight, 200 mg α-tocopherol/kg body weight, or 250 mg glycine betaine/kg body weight. Blood samples were collected to study the effect of Pb-toxicity on oxidative stress markers, liver enzymes, renal function, protein profile, activities of some antioxidant defensive enzymes, Pb+2 concentration in serum, and total calcium content in blood samples. the results can be summarized as follow: -
1. Effect of Pb-toxicity on albino rats metabolism: -
Treatment of albino rats with Pb-acetate (50 mg/kg bw/day) for 6 weeks resulted in significant changes in metabolic parameters included the following:
• Pb-acetate treatment resulted in a significant increase in the level of lipid peroxidation. MAD content in the Pb-intoxicated group was 7.84 times more than in the untreated control which reflects the fact that Pb-induces oxidative damage of cells, tissue, and organs after 6 weeks of Pb treatment.
• The reduced form of glutathione (GSH-R) was significantly decreased by Pb-treatment by 57% compared to untreated control. The reductive effect of Pb-toxicity on GSH-R confirms that oxidative stress could be one of the possible mechanisms of Pb-toxicity.
• Serum liver enzymes including AST, ALT, and ALP activities increased by 37.6%, 59,3, and 55.1% respectively. The obtained results proved that Pb-treatment induced hepatic toxicity.
• Exposure to Pb caused renal dysfunction where treatment with Pb-acetate resulted in significant increase in serum urea concentration by 23.7% after 6 weeks of treatment. Creatinine and uric acid insignificantly increased after 6 weeks of Pb-treatment. Increase renal parameters can be explained through the ability of Pb to induce ROS generation and renal damage in rats.
• Pb-toxicity caused a severe reduction in serum total protein, albumin, and globulin by 29.5%, 37.3%, and 20.8% respectively. The reductive effect of Pb on protein profile in serum could be attributed to its effect on renal function and /or excessive protein ¬¬¬¬¬¬¬¬-excretion and degradation.
• Administration of Pb (50 mg pb-acetate/kg. bw) for 6weeks caused significant inhibition in SOD, GPx, and GST by 75%, 40.8%, and 85%respectivly. The inhibitory effect of Pb on antioxidant/ detoxification enzymes indicated that Pb-toxicity induced pro. oxidant accumulation and caused oxidative stress.
• Treatment of male albino rats with Pb-acetate increased Pb+2and total calcium concentrations in serum by 5.9 times and 2.4% respectively compared to untreated control.
2. Effect of L-Ascorbic acid, α-tocopherol, and glycine betaine on Pb-intoxicated rats metabolism:
Treatment of Pb-intoxicated rats with 100 mg L-Ascorbic acid, 200 mg α-tocopherol, and 250 mg glycine betaine for 6 weeks mitigated Pb-toxicity through its effect on the following metabolic parameters: -
• L-Ascorbic acid and glycine betaine significantly reduced MDA content after 6 weeks of treatment while α-tocopherol treatment resulted insignificant slight decrease in MDA content compared to Pb-intoxicated rats.
• Glycine betaine treatment exhibited significant elevation in the level of reduced glutathione by 49.5%. On the other hand, treatment with either L-Ascorbic acid or α-tocopherol caused insignificant increases in reduced glutathione level by 28.4% or 12% respectively.
• Treatment of Pb-intoxicated rats with L-Ascorbic acid α-tocopherol and glycine betaine exhibited significant reduction in AST by 31.9%, 38.2%, 50.9% respectively. Also, ALT activity was decreased by 46.4%, 49.5%, 48.4% after treatment with L-Ascorbic acid, α-tocopherol, and glycine betaine respectively. L-Ascorbic acid treatment reduced ALP activity in Pb-intoxicated rats by 19.6% after 6 weeks of treatment. While treatment with α-tocopherol and glycine betaine increased ALP activity by 27% and 59.9% respectively.
• Treatment of Pb-intoxicated rats with L-Ascorbic acid, α-tocopherol and glycine betaine protected kidney and caused significant reduction in serum creatinine by 22.4%, 20%, and 26.8% respectively and reduced urea level to the level of untreated control. On the other hand, L-Ascorbic acid, α-tocopherol, and glycine betaine did not exhibited in any significant changes in uric acid content in Pb-intoxicated rats.
• Supplementation of Pb-intoxicated rats with L-Ascorbic acid, α-tocopherol, and glycine betaine significantly increased the concentrations of serum total protein, albumins, and globulins. The protective effect of L-Ascorbic acid, α-tocopherol, and glycine betaine on protein profile in Pb-intoxicated rats could be attributed to their capacity to protect kidney cellular membranes from lipid peroxidation and subsequently reduction of protein excessive excertion during Pb-poisoning.
• SOD, GPx, and GST activities significantly activated after 6 weeks of treatment with L-Ascorbic acid, α-tocopherol, and glycine betaine. GB was found to be the most effective treatment which increased the activities of SOD, GPx, and GST by 27.0%. 40.8%, and 63.9% respectively after 6 weeks of treatment.
• Pb+2 was reduced after 6 weeks after of treatment with L-Ascorbic acid, α-tocopherol, and glycine betaine by 32.1%30%, and 57.5% respectively. While total calcium level was increased by treatment with L-Ascorbic acid and glycine betaine. In contrast α-tocopherol treatment caused significant reduction in total calcium level to reach the level of untreated control (G1).
The previous results concluded that L-Ascorbic acid, α-tocopherol, and glycine betaine can be used to mitigate the harmful effects of Pb-toxicity in male albino rats. The detoxification characteristics of L-Ascorbic acid, α-tocopherol, and glycine betaine could be due to their antioxidant activity and their ability to induce antioxidant defensive enzymes activities and chelate the harmful Pb+2. The most effective treatment in mitigation of Pb-toxicity was glycine betaine treatment (250mg GB/Kg bw). Our Data extremely recommended administration of vitamin C, vitamin E, and GB as natural protectants against Pb-toxicity in high contaminated regions with Pb.