scholarly journals Beneficial Effect Administration of Vitamin C in Amelioration of Lead Hepatotoxicity

2012 ◽  
Vol 4 (3) ◽  
pp. 07-13 ◽  
Author(s):  
Nadia AIT HAMADOUCHE ◽  
Miloud SLIMANI ◽  
Abdelkader AOUES
Keyword(s):  
Lipid Peroxidation ◽  
Drinking Water ◽  
Vitamin C ◽  
Lead Acetate ◽  
Metal Content ◽  
Protective Action ◽  
Venous Blood ◽  
Lipid Hydroperoxide ◽  
Experimental Studies ◽  
Male Rats

Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipid. Oxidative stress with subsequent lipid peroxidation has been postulated as one mechanism for lead toxicity. The protective action of vitamins C against lead affects lipid hydroperoxide level and liver functions in male rats has been studied. Experiments were performed on male waster rats with body weights of 120-160 g. Male wistar rats were exposed to 3 g/l lead acetate in drinking water for 5 weeks and treated thereafter with vitamin C (500 mg/kg, orally) for 28 days. One day after the feeding was over, venous blood samples, under chloroform anesthesia, were collected. The animals were killed by exsanguinations and the liver was excise for determination the metal content and histopathological changes. Similarly, the tissue lipid (lipid peroxidation) and the enzyme fraction (superoxide dismutase (SOD), catalase (CAT), alkaline phosphatase (ALP), acid phosphatase (ACP) and glutathione (GSH) were also measured in the liver. Metal content in blood and liver was determined by means of atomic absorption spectrophotometry. Administration of lead acetate (3 g/l) in drinking water for 5 weeks induced a significant increase in the levels of hepatic ALP, ACP and lipid peroxidation. Lead acetate exposure also produced detrimental effects on the redox status of the liver indicated by a significant decline in the levels of liver antioxidants such SOD, CAT and GSH. Further, there was a significant increase in the levels of lead in blood and liver of animals exposed to lead. However, oral administration of vitamin C at dose level of 500 mg/kg body weight reduced the alterations in the previous parameters. Histological examination of the liver also revealed pathophysiological changes in lead acetate-exposed group and treatment with vitamin C improved liver histology. The result of this study strongly indicate that vitamin C has got a potent antioxidant action against lead acetate induced hepatic damage in rats.

scholarly journals Impact of lead acetate and sodium and potassium stearates on lipid peroxidation processes in the body of experimental animals

2021 ◽  
Vol 100 (4) ◽  
pp. 406-410
Author(s):  
Olha Ye. Fedoriv ◽  
Alexandra Ye. Kopach ◽  
Nataliia A. Melnyk
Keyword(s):  
Lipid Peroxidation ◽  
Drinking Water ◽  
Lead Acetate ◽  
Sodium Stearate ◽  
The Body ◽  
Female Rats ◽  
White Female ◽  
Control Group ◽  
Diene Conjugates ◽  
Group 2

Introduction. Given the significant prevalence of lead in the environment, research in this area has significant social and economic importance. Lead compounds are characterized by high toxicity and increased ability to cumulate in ecosystems, humans, and animals. Lead enters the human body with food, drinking water, atmospheric air, and smoking. Lead causes pathological changes in the nervous system, blood-forming organs, kidneys, etc. Materials and methods. The experiments were carried out on four groups of white female rats, each included seven animals, weighing 150-200 g. The first group of animals was a control. The second group consumed dechlorinated water from the city water supply, followed by lead acetate. The animals from the third and fourth groups drank the same water with sodium stearate and potassium stearate content in a dose of 1/250 LD50. After the 40th-day of the use of these waters, the animals were orally administered lead acetate at a dose of 7 mg/kg. The levels of lipid peroxidation biomarkers were studied by studying the content of diene conjugates (DC) and malondialdehyde (MDA) in blood serum, liver, and kidney homogenates. Results. The administration of 1/2 acetate LD50 to lead in experimental rats drinking water with stearates was accompanied by a significant increase in the DCs concentration and (MDA) in animals. Higher concentrations of LPO products were observed in the group of animals that consumed water from potassium stearate. Conclusions. 1. With the oral administration of lead acetate against the background of drinking water containing stearates at a dose of 1/250 LD50, an increase in lipid peroxidation indices was noted compared with the control group. 2. Higher concentrations of LPO products were observed in the group of animals consuming water from potassium stearate.

Cytoprotective Effects of Zingiber officinale Against the Oxidative Stress Induced by Lead Acetate Toxicity in Rats

2020 ◽  
Author(s):  
O. Aouacheri ◽  
S. Saka
Keyword(s):  
Oxidative Stress ◽  
Drinking Water ◽  
Lead Acetate ◽  
Zingiber Officinale ◽  
Treated Group ◽  
Normal Diet ◽  
Male Rats ◽  
Control Group ◽  
Experimental Diet ◽  
Group I

The evaluation of the effect of ginger on the modulation of toxic effects induced by lead is the objective of our study. Forty male rats were randomly divided into four groups and treated daily for 3 consecutive months. Group I (0-0) was kept as control; group II (0-G) received an experimental diet with 2% of ginger; group III (Pb-0) received 2% lead acetate dissolved in drinking water with a normal diet; and group IV (Pb-G) received 2% lead acetate in drinking water and an experimental diet containing 2% ginger. Lead acetate exposure caused a significant increase of organosomatic indexes, hepatic, lipid, and urine profiles. In addition, lead acetate has a pro-oxidative effect expressed by a significant decrease in tissue GSH levels and the enzymatic activity of GPx and CAT. This pro-oxidative action was also marked by an increase in MDA level and GST activity in lead-treated group. Feeding ginger-supplemented diet to lead acetate-treated rats restored all the parameters studied as compared to control. These results suggest that ginger treatment exerts a protective effect on metabolic disorders by decreasing the oxidative stress.

scholarly journals Protective role of ascorbic acid on lead-induced damage to the thyroid gland in the rat

2020 ◽  
Vol 9 (5) ◽  
pp. 632-635
Author(s):  
Denisse Calderón-Vallejo ◽  
María del Carmen Díaz-Galindo ◽  
Andrés Quintanar-Stephano ◽  
Carlos Olvera-Sandoval ◽  
J Luis Quintanar
Keyword(s):  
Ascorbic Acid ◽  
Drinking Water ◽  
Thyroid Gland ◽  
Lead Poisoning ◽  
Lead Acetate ◽  
Protective Action ◽  
Protective Role ◽  
Thyroid Stimulating Hormone ◽  
Stimulating Hormone

Abstract Lead exposure is known to affect the pituitary-thyroid axis. Likewise, ascorbic acid (AA) has a protective action against lead poisoning. We examine the protective role of AA in lead-induced damage to the thyroid gland. The Wistar rats were divided into three groups: control that received 0.2% AA in drinking water throughout the experiment (15 days), intoxicated with lead acetate (20 mg/kg) intraperitoneally every 48 h for 15 days, and the experimental group treated with lead acetate and 0.2% AA in drinking water throughout the experiment. Plasma thyroid-stimulating hormone, triiodothyronine, thyroxine, and lead were determined. The thyroid gland was weighed, then epithelial cell height and nuclear volume were measured on histological slides. The results show that AA reduced the thyroid atrophy caused by lead acetate, as well as the loss of weight of the gland. In addition, it prevented the decrease of the hormone triiodothyronine, although the thyroxine hormone remained lower than the control values ​​and the thyroid-stimulating hormone remains high. Our results indicated that AA could play a protective role in lead poisoning in the thyroid gland.

Aqueous extract of Pedalium murex D. Royen ex L. leafy stem protects against lead induced testicular toxicity in Wistar rats

2022 ◽  
Vol 0 (0) ◽  
Author(s):  
Gerard Bessan Dossou-Agoin ◽  
Adam Gbankoto ◽  
Simon Azonbakin ◽  
Razack Osseni ◽  
Achille Yemoa ◽  
...  
Keyword(s):  
Drinking Water ◽  
Aqueous Extract ◽  
Lead Acetate ◽  
Semen Quality ◽  
Male Rats ◽  
Seminiferous Tubules ◽  
Testicular Toxicity ◽  
Male Reproductive Function ◽  
Stem Extract ◽  
Pedalium Murex

Abstract Objectives Lead exposure seriously impairs male reproductive function. The protective capacity of Pedalium murex leafy stem and fruit aqueous extracts against lead testicular toxicity is evaluated to find herbals drugs able to improve semen quality. Methods Phytochemical screening were performed according to classical methods. Twenty four male rats were divided into four groups of six rats each and received the following treatments via oral route: distilled water; 0.2% lead acetate in drinking water; 0.2% lead acetate in drinking water with 400 mg/kg P. murex aqueous leafy stem extract; 0.2% leaded water with 400 mg/kg P. murex aqueous fruit extract. Treatments were administered for 70 days. Body and reproductive organs weights, sperm parameters and testicular histological sections of each group were examined. Results Flavonoids, tannins, coumarins, alkaloids, and lignans were found in both extracts. Lead intoxication reduced sperm motility and count but increased the percentage of morphologically abnormal sperms. The germinal epithelium of seminiferous tubules histoarchitecture was disorganized by lead. The leafy stem extract was effective in reducing lead induced testicular disruption whereas fruit has not shown any beneficial effect. Conclusions P. murex leafy stem aqueous extract is effective against semen alterations caused by lead.

Effect of chronic fluorosis on lipid peroxidation and histology of lung tissues in first and second generation rats

2006 ◽  
Vol 22 (9) ◽  
pp. 375-380 ◽  
Author(s):  
Meral Oncu ◽  
Kanat Gulle ◽  
Erdal Karaoz ◽  
Fatih Gultekin ◽  
Sureyya Karaoz ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Drinking Water ◽  
First Generation ◽  
Second Generation ◽  
Experimental Period ◽  
Male Rats ◽  
Lactation Period ◽  
Pregnant Rats ◽  
Chronic Fluorosis ◽  
First And Second Generation

This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first and second generation rat lung tissues. Sixteen, virgin, female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two experimental groups (control and fluoride supplemented). The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and lactation periods. After the lactation period, young animals (first generation; F1) were exposed to the same amount of NaF in drinking water for four months. At the end of the four-month experimental period, nine randomly-chosen male rats (F1) were sacrificed and lung tissues were removed for histopathological and enzymatic lipid peroxidation examination. The second generation rats were obtained from the remaining rats by the same method. They were also treated similarly. At the end of the four-month experimental period, nine randomly-chosen male rats (F2) were sacrificed, and the lungs were removed for histological and lipid peroxidation examination. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and the lung TBARS levels of fluoride supplemented F1 and F2 rats were higher than controls. There were marked histological changes in the lung tissues of fluoride supplemented F1 and F2 rats, as follows: in F1 rats; loss of alveolar architecture, emphysematous areas, descuamation of alveolar epithelium and alveolar congestion were observed. There were thickened interalveolar septae and congestion of alveolar septal vessels. Intraparenchymal thick-walled vessels were also observed. There were markedly perivascular and intraparenchymal focal mononuclear cell infiltrations. In F2 rats, in addition to these changes, there were lipid cell hyperplasia and increased connective tissue mass in the parenchymal areas. It is concluded that chronic fluorosis causes a marked destruction in lung tissues of F1 and F2 rats by causing lipid peroxidation. Toxicology and Industrial Health 2006; 22: 375-380.

scholarly journals Vitamin C and Turmeric Attenuate Bax and Bcl-2 Proteins’ Expressions and DNA Damage in Lead Acetate-Induced Liver Injury

Dose-Response ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 155932581988578 ◽  
Author(s):  
Ahlam M. Alhusaini ◽  
Laila M. Faddah ◽  
Iman H. Hasan ◽  
Somayah J. Jarallah ◽  
Shrouq H. Alghamdi ◽  
...  
Keyword(s):  
Vitamin C ◽  
Lead Acetate ◽  
Weight Ratio ◽  
B Cell Lymphoma ◽  
Male Rats ◽  
Protective Effects ◽  
Body Weight Ratio ◽  
Hepatic Lipid Peroxidation ◽  
Hematoxylin And Eosin ◽  
Vit C

Background: Lead is a common environmental and occupational pollutant which induced multiorgans dysfunction. The present study was designed to investigate the hepatoprotective effects of turmeric (TUR) and/or vitamin C (Vit-C) alone or together against lead acetate toxicity and to explore novel molecular pathways. Method: Acute hepatotoxicity was induced by lead acetate (100 mg/kg/day, i.p.) in male rats, and the effect of TUR (200 mg/kg/day, orally) and/or Vit-C (250 mg/kg/day, orally) along with lead acetate for 7 days was studied. Results: Lead acetate increased serum alanine transaminase, aspartate transaminase, lactate dehydrogenase, hepatic lipid peroxidation and nitric oxide; while, hepatic superoxide dismutase and glutathione activities were downregulated. Hepatic Bcl-2-associated X (Bax) and B-cell lymphoma-2 (Bcl-2) proteins expressions were altered and hepatic DNA damaged was increased as well. Liver/body weight ratio was decreased. Hematoxylin and eosin demonstrated that lead acetate induced focal areas of massive hepatic degeneration of the hepatocytes. Treatment with both antioxidants ameliorated all the altered parameters and induced marked improvement of liver architecture. Conclusion: The combination of TUR and Vit-C has shown the most protective effects against lead acetate-induced hepatotoxicity.

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