Methamphetamine and lipid peroxidation in the rat retina
Article first published online: 6 MAY 2005
Copyright © 2005 Wiley-Liss, Inc.
Birth Defects Research Part A: Clinical and Molecular Teratology
Volume 73, Issue 6, pages 455–460, June 2005
How to Cite
Melo, P., Rodrigues, L. G., Pinazo-Durán, M. D. and Tavares, M. A. (2005), Methamphetamine and lipid peroxidation in the rat retina. Birth Defects Research Part A: Clinical and Molecular Teratology, 73: 455–460. doi: 10.1002/bdra.20138
- Issue published online: 2 JUN 2005
- Article first published online: 6 MAY 2005
- Manuscript Accepted: 27 JAN 2005
- Manuscript Received: 11 AUG 2004
- Sponsoring program from Fundaçia Ciençia e Tecnologia (PRAXIS). Grant Numbers: XXI/BD/3395/2000, XXI/BD/18508/98
- Instituto de Salud Carlos III, Programa de Financiamento Plurianual do Instituto Biologia Molecular e Celular (IBMC)
- Instituto de Salud Carlos III, Fundo Europeu Desenvolvimento Regional (FIS-FEDER). Grant Number: P10 20191
- lipid peroxidation;
- oxidative stress;
The use of psychoactive drugs during adolescence and early adult life has increased in the last few decades. It is known that developmental exposure to psychostimulants affects the sensory systems, and the retina has been shown to be a target tissue. This work was conducted to evaluate the pattern of lipid peroxidation in the rat retina following prenatal exposure to methamphetamine (MA).
Pregnant female Wistar rats were given MA (5 mg/kg of body weight/day; SC, in 0.9% saline) from GD 8 to 22. Offspring were sacrificed at postnatal days (PNDs) 7, 14, and 21. The retinas were homogenized, and both the total antioxidant and superoxide dismutase (SOD) activities were measured by enzymatic-colorimetric methods. The lipid peroxidation byproducts (malondialdehyde [MDA] and MDA-like metabolites) were measured by the thiobarbituric acid test.
Total antioxidant levels were lower in the MA group at PND 21 in both males and females. The activity of SOD was higher in PND 7 females from the MA group. MDA levels were higher in the MA group at PND 21 in both genders.
These findings suggest that prenatal-induced MA toxicity in the retina may be related to lipid peroxidation processes and oxidative stress. Birth Defects Research (Part A), 2005. © 2005 Wiley-Liss, Inc.