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. 2003 Apr;44(3):417-20.
doi: 10.1007/s00244-002-2023-4.

Oxidative effects of lead in young and adult Fisher 344 rats

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Oxidative effects of lead in young and adult Fisher 344 rats

N Aykin-Burns et al. Arch Environ Contam Toxicol. 2003 Apr.

Abstract

Lead poisoning has been extensively studied over the years. Many adverse physiological and behavioral impacts on the human body have been reported due to the entry of this heavy metal. It especially affects the neural development of children. The current study investigates the effect of lead exposure in young (1.5 months) and adult (10 months) male Fisher 344 rats. Five weeks of lead administration resulted in a profound change in the lead levels in the red blood cells (RBCs) of the young lead-exposed group (37.0 +/- 4.47 microg/dl) compared to the control (<1 microg/dl) and adult (27.4 +/- 8.38 microg/dl) lead-exposed groups. Therefore, this study confirms the fact that gastrointestinal absorption of lead in young is greater than that of adults. Furthermore, glutathione and glutathione disulfide (GSSG) levels in RBCs, liver, and brain tissues were measured to determine thiol status; malondialdehyde (MDA) levels of lipid peroxidation and catalase activity were measured to assess changes in oxidative stress parameters. Liver GSSG and MDA levels were significantly higher in the young lead-exposed group than those in the adult lead-exposed group. In RBCs and brains, however, adult lead-exposed animals have shown more elevated MDA levels than young animals exposed to the same lead treatment.

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Figures

Figure 1
Figure 1
Schematic Representation of the Steps in Lipid Hydroperoxide (LHP) Assay
Figure 2
Figure 2
Cytotoxicity of lead nitrate to human leukemia (HL-60) cells
Figure 3
Figure 3
LHP standard curve showing the net absorbance at 586 nm as a function of lipid hydroperoxide concentration.
Figure 4
Figure 4
Effects of different concentrations of lead nitrate on LHP generation in HL-60 cells.

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References

    1. Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profile for Lead. Public Health Service, U.S. Department of Health and Human Services; Atlanta, GA: 1999.
    1. Hermes-Lima M, Valle VGR, Vercesi AE, Bechara EJH. Damage to rat liver mitochondria promoted by δ-aminolevulinic acid-generated reactive oxygen species: connections with acute intermittent porphria and lead poisoning. Biochim Biophys Acta. 1991;1056:57–63. - PubMed
    1. Tchounwou PB, Yedjou CG, Foxx D, Ishaque A, Shen E. Lead induced cytotoxicity and transcriptional activation of stress genes in human liver carcinoma cells. Mol Cell Biochem. 2004;255:161–170. - PubMed
    1. Tully DB, Collins BJ, Overstreet JD, Smith CS, Dinse GE, Mumtaz MM, Chapin RE. Effects of arsenic, cadmium, chromium and lead on gene expression regulated by a battery of 13 different promoters in recombinant HepG2 cells. Toxicol Appl Pharmacol. 2000;168:79–90. - PubMed
    1. Tchounwou PB, Yedjou CG, Dorsey WC. arsenic trioxide induced transcriptional activation and expression of stress genes in human liver carcinoma cells (HepG2) Cellular and Molecular Biology. 2003;49(7):1071–1079. - PubMed

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