Lead intoxication: Histological and oxidative damage in rat cerebrum and cerebellum

Sidhu, Pardeep; Nehru, Bimla

doi:10.1002/jtra.10052

Cited by 59 publications

(48 citation statements)

References 30 publications

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“…Many animal studies have shown that lead is capable of causing oxidative stress in the kidney, liver, and brain (Ercal et al, 1996;Patra et al, 2001). The absorbed Pb is conjugated in the liver and passed to the kidney, where a small quantity is excreted in urine and the rest accumulates in various body organs, affecting and affects many biological activities at the molecular, cellular and intercellular levels, which may result in morphological alterations that can remain even after Pb levels have fallen (Jarrar, 2003;Sidhu & Nehru, 2004;Taib et al, 2004;Flora et al, 2006). The kidney is a sensitive target organ for lead exposure.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural Changes in the Kidney Cortex of Rats Treated with Lead Acetate

et al. 2011

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SUMMARY:The purpose of this study was to investigate the ultrastructural effects of lead on the kidney cortex of rats. Wistar Albino rats (180-200g body weight) were divided into a controlled and lead acetate-exposed group. Rats received lead acetate at 500 ppm in their drinking water for 60 days. Both groups were fed with the same standard food, but lead acetate was added to the drinking water. During the experimental period, blood samples were taken from the abdominal aorta of the anesthetised animals. At the end of exposure, body weight and blood lead levels were measured. The kidney tissue samples were prepared and analyzed by light and transmission electron microscopy. Cortical renal tubules show various degenerative changes with focal tubular necrosis invaded by inflammatory cells. The ultrastructural alterations found in lead acetate-treated rats were a diminution in the amount of filtration slits, increased fusion of foot processes in epithelial cells of the glomeruli, increase of lysosomal structures and pinocytic vesicles as well as large mitochondria in proximal tubule cells.

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Section: Introductionmentioning

confidence: 99%

Ultrastructural Changes in the Kidney Cortex of Rats Treated with Lead Acetate

et al. 2011

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“…Studies have shown that lead damages the nerve cells as well as ganglia and also alters the cell structure causing cerebral edema, and focal cerebellar atrophy and neuronal degeneration as a result of lead encephalopathy in rat brain [69] . Treatment with omega-3FA has been found to restore cellular functions, reduce oxidative stress and inflammation, repair cellular damage and mitigate the activation of apoptotic processes after traumatic brain injury in human [71] .…”

Section: Doi: 101159/000481808mentioning

confidence: 99%

“…Exposure to lead in rats affects the normal histological structure of the brain and causes disturbances in the normal functions performed by it. Lead toxicity also damages the nerve cells and ganglia linked with the damage of cellular structure as well as the neuronal degeneration as a result of lead encephalopathy in rat brain [69,70] .…”

Section: Doi: 101159/000481808mentioning

confidence: 99%

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Singh

Yadav

et al. 2017

Ann Neurosci

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Background: Lead is widely distributed in the environment and has been found to be associated with various health problems including neurodegenerative diseases. Purpose: In view of the increasing health risk caused by lead, this study has been carried out to investigate the neuroprotective effect of omega-3 fatty acid (omega-3FA) in lead-induced neurotoxicity in rats. Methods: Biochemical parameters including oxidative stress in brain regions, lead levels in blood and brain regions and histopathological examination of brain regions of rats were carried out in the present study. Results: Rats exposed to lead (lead acetate 7.5 mg/kg body weight p.o. for 14 days) caused a significant increase in the levels of lipid peroxidation, protein carbonyl content, ROS production and decreased the activities of glutathione peroxidase, superoxide dismutase and catalase in the cerebellum and cerebral cortex, respectively, as compared to controls. Abnormal histopathological changes and increase in the levels of lead in blood and brain were also observed as compared to controls. Co-treatment of lead with omega-3FA (750 mg/kg body weight p.o. for 14 days) decreased the levels of lipid peroxidation, protein carbonyl content, ROS production and increased the activities of glutathione peroxidase, superoxide dismutase and catalase and showed protection in the histopathological study as compared to rats treated with lead alone. Conclusions: The result of the present study shows that lead-induced oxidative stress and histopathological alteration in the brain region were significantly protected with co-treatment of lead and omega-3FA. This could be due to its strong antioxidant potential and metal-binding property.

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“…[4] This affects many biological activities at the molecular, cellular and intercellular levels, which may result in morphological alterations that can remain even after lead level has fallen. [5,6,7,8] Lead element is one of the most common toxic metal and affects all organs of the body including liver. Liver is the largest organ in the body and it is located in the upper three regions in the abdomen.…”

Section: Introductionmentioning

confidence: 99%

Lead Acetate Effects on Hepatocyte Degeneration in Chick Embryo Liver

Kedam¹

2017

WJPPS

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The liver is considered as one of the target organs affected by lead toxicity owing to its site of storage after exposure. Liver is a primary organ involved in the biotransformation and detoxification of toxic substances. Inhalation and ingestion of lead are the most common routes of exposure. Absorbed lead is stored in liver via the portal vein, for this reason the study was conducted to describe the histological changes after lead exposure in developing chick embryo. The lead acetate treated chick embryo liver during development has acquired modification of normal to necrosed structure. The necrosed liver under microscopy showed congestion, elongated sinusoidal spaces and degenerated hepatocytes. Hence the present study concludes that the lead as heavy metal causes damage to liver and hepatocytes.

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Lead intoxication: Histological and oxidative damage in rat cerebrum and cerebellum

Cited by 59 publications

References 30 publications

Ultrastructural Changes in the Kidney Cortex of Rats Treated with Lead Acetate

Ultrastructural Changes in the Kidney Cortex of Rats Treated with Lead Acetate

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Lead Acetate Effects on Hepatocyte Degeneration in Chick Embryo Liver

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