Oxidative Damage of Cardiovascular System in Rats Following Lead Exposure

Article Preview

Abstract:

The aim of the current study is to figure out the relationship between the oxidative damage in cardiovascular system and lead exposure. Oxidative damage was investigated in the heart and aorta of rats exposed to lead acetate for 6 weeks. Male wistar rats were randomly divided into three groups: low-dose (10 mg/kg), high-dose (40 mg/kg) lead acetate and control groups. The rats in low-, or high-dose groups were received 10 mg/kg and 40 mg/kg lead acetate by garages, and the rats in control group were administrated same amount distilled water only. We compared the three groups in terms of the level of T-SOD, NOS, and MDA in serum and heart, aorta and histological examination. We found the activity of T-SOD, NOS in rats treated with low and high doses of lead acetate were significantly lower than in the control group. The content of MDA in the low and high doses of lead acetate groups was significantly higher than in the control group. In addition, the microscopic morphology of heart and aorta in the low- and high-dose groups showed differences from the control. Oxidative damage may be involved in the process of heart and aorta dysfunction induced by lead exposure.

You might also be interested in these eBooks

Info:

Periodical:

Pages:

987-991

Citation:

Online since:

February 2011

Export:

Price:

Permissions CCC:

Permissions PLS:

Сopyright:

© 2011 Trans Tech Publications Ltd. All Rights Reserved

Share:

Citation:

[1] Pirkle, J.L., Brody, D.J., Gunter, E.W., et al.: The decline in blood lead levels in the United States. The National Health and Nutrition Examination Surveys (NHANES). JAMA 272(4), 284–291(1994).

DOI: 10.1001/jama.1994.03520040046039

Google Scholar

[2] Bhatnagar, A.: Environmental cardiology: studying mechanistic links between pollution and heart disease. Circ Res 99(7), 692–705(2006).

DOI: 10.1161/01.res.0000243586.99701.cf

Google Scholar

[3] Weinhold B.: Environmental cardiology: getting to the heart of the matter. Environ Health Perspect 112(15), A880–887(2004).

Google Scholar

[4] Menke, A., Muntner, P., Batuman, V., et al.: Blood lead below 0. 48 micromol/L (10 microg/dL) and mortality among US adults. Circulation. 114(13), 1388-1394(2006).

DOI: 10.1161/circulationaha.106.628321

Google Scholar

[5] Navas-Acien, A., Selvin, E., Sharrett, A.R., et al.: Lead, cadmium, smoking, and increased risk of peripheral arterial disease. Circulation 109(25), 3196–3201(2004).

DOI: 10.1161/01.cir.0000130848.18636.b2

Google Scholar

[6] Schober, S.E., Mirel, L.B., Graubard, B.I., et al. Blood lead levels and death from all causes, cardiovascular disease, and cancer: results from the NHANES III Mortality Study. Environ Health Perspect 114(10), 1538–1541(2006).

DOI: 10.1289/ehp.9123

Google Scholar

[7] Sennoun, N., Meziani, F., Dessebe, O., et al.: Activated protein C improves lipopolysaccharide- induced cardiovascular dysfunction by decreasing tissular inflammation and oxidative stress. Crit Care Med 37(1), 246-255(2009).

DOI: 10.1097/ccm.0b013e318192fe4f

Google Scholar

[8] Yu, M.A., Sánchez-Lozada, L.G., Johnson, R.J., et al.: Oxidative stress with an activation of the renin-angiotensin system in human vascular endothelial cells as a novel mechanism of uric acid-induced endothelial dysfunction. J Hypertens 28(6), 1234-1242(2010).

DOI: 10.1097/hjh.0b013e328337da1d

Google Scholar

[9] Gautam, P., Flora, S.J.: Oral supplementation of gossypin during lead exposure protects alteration in heme synthesis pathway and brain oxidative stress in rats. Nutrition 26(5), 563-570(2010).

DOI: 10.1016/j.nut.2009.06.008

Google Scholar

[10] Bhatti, P., Stewart, P.A., Hutchinson, A.: Lead exposure, polymorphisms in genes related to oxidative stress, and risk of adult brain tumors. Cancer Epidemiol Biomarkers Prev 18(6), 1841-1848(2009).

DOI: 10.1158/1055-9965.epi-09-0197

Google Scholar

[11] Cai, H., Harrison, D.G.: Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress. Circ Res 87(10), 840–844(2000).

DOI: 10.1161/01.res.87.10.840

Google Scholar