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Lead intoxication has been a major health hazard in humans. It affects people at all ages. Its toxicity is associated with various organs of the body and affects different metabolic pathways. Based on histological data, l-carnitine reduced the severity of tissue damage produced as a result of exposure of rats to lead acetate. The main objective of this study was to evaluate the underlying mechanism of protection offered by l-carnitine against lead acetate intoxication using male Sprague-Dawley rats. Forty male Sprague-Dawley rats were randomly divided into four groups with ten rats in each. The first group (G1) served as the control group and animals received standard diet only. The second group (G2) received lead acetate in their diet. The third group (G3) was the l-carnitine treated group and received the normal standard diet supplemented with l-carnitine. While the fourth group (G4) had a diet supplemented with both lead acetate and l-carnitine. At the end of each experiment, blood (serum and whole blood) were collected from each animal and analyzed for the following parameters: serum testosterone levels, serum nitric oxide and serum malondialdehyde. This is in addition to looking at the enzymatic activities of two important enzymes (superoxide dismutase and catalase) and on (glutathione reductase) which are indicative of the antioxidant activities in the whole blood. The results indicated that l-carnitine will counteract the undesirable effects of lead intoxication. It exerted its antioxidant potential by reducing the production of ROS and scavenging free radicals by maintaining and protecting the level of the of antioxidant enzymes SOD, CAT and glutathione peroxidase. l-Carnitine may play an important role in reversing the undesirable effects of lead intoxication. Future studies should be conducted to see whether such an effect is applicable in humans exposed to lead poising.
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http://dx.doi.org/10.1016/j.sjbs.2016.08.010 | DOI Listing |
Int J Phytoremediation
December 2024
Department of Botany, Sree Neelakanta Government Sanskrit College, Pattambi, India.
Anthropogenic activities have accelerated lead (Pb) accumulation across different trophic levels in the ecosystem. This study focused on the physiological mechanisms of an invasive plant, in a controlled hydroponic setting to understand its response to Pb stress. was exposed to 680 µM of lead acetate for 21 days, showing high tolerance (83%) with minimal growth inhibition.
View Article and Find Full Text PDFJ Toxicol
November 2024
Department of Pathobiology, Sanandaj Branch, Islamic Azad University, Sanandaj, Iran.
Lead, a heavy metal, has emerged as one of the most significant pollutants, bearing irreversible consequences on human and animal health in conjunction with industrial development. Presently, the use of medicinal plants to alleviate the adverse effects of heavy metal toxicity has captured the attention of researchers. Hence, the objective of this study was to assess the impact of levamisole and broccoli extract on the electrophoretic pattern of serum proteins, hematological parameters, and histopathological alterations in the liver, kidney, and spleen tissues within a lead poisoning model of rats.
View Article and Find Full Text PDFEcotoxicol Environ Saf
December 2024
Department of Theriogenology, Faculty of Veterinary Medicine, Suez Canal University, Ismailia 41522, Egypt.
Birth Defects Res
December 2024
Department of Zoology, University of Sargodha, Sargodha, Punjab, Pakistan.
Neurotoxicology
December 2024
Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China. Electronic address:
Mitochondria is the primary target of lead (Pb) in neural cells, and Pb exposure can cause impairment to mitochondrial function and morphology. Recent studies have reported that a conserved cellular stress response, called mitochondrial unfolded protein response (mtUPR), is activated in response to mitochondrial dysfunction and protein misfolding and play protective roles in aging and neurodegeneration, but it's unknown whether mtUPR could protect against Pb-induced neurotoxicity. In this study, we found that sublethal level exposure of PbAc (2.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!