This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Soltaninejad, K. Articles by Abdollahi, M. Search for Related Content PubMed PubMed Citation Articles by Soltaninejad, K. Articles by Abdollahi, M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB LEAD ACETATE LEAD COMPOUNDS MALONALDEHYDE Medline Plus Health Information Lead Poisoning Social Bookmarking                         What's this?

Biochemical and ultrastructural evidences for toxicity of lead through free radicals in rat brain

Abbas Kebriaeezadeh

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Science, Tehran, Iran

Bagher Minaiee

Department of Histology, Faculty of Medicine, Tehran University of Medical Science, Tehran, Iran

Seyed Naser Ostad

Ruhollah Hosseini

Ebrahim Azizi

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Science, Tehran, Iran

Mohammad Abdollahi

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Science, Tehran, Iran; Faculty of Pharmacy, Tehran University of Medical Science, Tehran 14155-6451, Iranmohammad.abdollahi{at}utoronto.ca

Studies suggest that some lead-induced toxic effects may occur through free radical production and oxidative stress. This study examined the relationship between brain histopathological alterations and oxidative stress in subchronic lead exposure. Male Albino rats received lead acetate at 0.01%, 0.05% and 0.1% w/v in their drinking water for 30 days. Animals given sodium acetate (0.1% w/v) served as control in the same period. At the end of exposure, blood-lead levels, blood catalase (CAT) and superoxide dismutase (SOD) activities and malondialdehyde (MDA) content (in blood and brain) were measured. The brain tissue samples were prepared and analysed by light and scanning electron microscopy. The results show that, the blood-lead levels in treated animals were higher in comparison with control. CAT and SOD activities in animals treated with 0.01% and 0.05% w/v did not increase in comparison with control (P>0.05) but these values were higher in animals treated with 0.1% w/v lead acetate (P<0.01). MDA content in blood and brain of animals treated with lead acetate 0.1% w/v, increased significantly (P<0.01), but these values were not significantly increased in other treated animals. No major histopathological alterations were detected in the brains of animals treated with lead acetate at 0.01% and 0.05% w/v. In animals treated with lead acetate 0.1% w/v, demyelinization and collagenous scar formation with neuronal atrophy in hippocampus region was observed. It is concluded that lead acetate induce oxidative stress which has an important role in brain damage in rats.

Key Words: brain • free radical • lead • oxidative stress • rat

Human & Experimental Toxicology, Vol. 22, No. 8, 417-423 (2003)
DOI: 10.1191/0960327103ht385oa


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				I. H El-Sayed, M. Lotfy, O.-A. Y El-Khawaga, W. A Nasif, and M. El-Shahat Prominent free radicals scavenging activity of tannic acid in lead-induced oxidative stress in experimental mice Toxicology and Industrial Health, May 1, 2006; 22(4): 157 - 163. [Abstract] [PDF]

				S. Kasperczyk, E. Birkner, A. Kasperczyk, and J. Kasperczyk Lipids, lipid peroxidation and 7-ketocholesterol in workers exposed to lead Human and Experimental Toxicology, June 1, 2005; 24(6): 287 - 295. [Abstract] [PDF]