[Frontiers in Bioscience 12, 1174-1183, January 1, 2007]

Oxidative damage lipid peroxidation in the kidney of choline-deficient rats

Georgina Ossani 1, Marianela Dalghi 2 and Marisa Repetto 2

1 Centro de Patología Experimental, Departamento de Patología, Facultad de Medicina and 2 Laboratorio de Estrés Oxidativo y Canales Iónicos, Cátedra de Química General e Inorgánica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Spain


1. Abstract
2. Introduction
3. Materials and methods
3.1. Animals
3.2. Histophatology
3.3. Tissue homogenate preparation
3.4. Mitochondria, plasma membrane and lysosomes.
3.5. Tert-butyl hydroperoxide-initiated chemiluminescence
3.6. Malondialdehyde determination
3.7. Protein determination
3.8. Chemicals
3.9. Statistical analysis
4. Results
5. Discussion
6. Perspectives
7. Acknowledgments
8. References


Phosphatidylcholine is the most abundant phospholipid constituent of cell membranes and choline is a quaternary amine required for phosphatidylcholine synthesis. The impairment of membrane functions is considered as an indication of oxidative damage. In order to kinetically analyze the time course of the pathogenesis of renal necrosis following to choline deficiency in weanling rats, we determined markers of membrane lipid peroxidation (thiobarbituric acid reactive substances; TBARS and hydroperoxide-induced chemiluminescence (BOOH-CL) ) and studied the histophatological damage. Plasma TBARS (t = 2.5 days) was an early indicator of systemic oxidative stress, likely involving liver and kidney. The levels of TBARS an BOOH-CL increased by 80 % and by 183 %, respectively, in kidney homogenates with t = 1.5 days and 4 days, respectively. The levels of BOOH-CL were statistically higher in rats fed a choline-deficient diet at day 6, in a mixture of membranes (from plasmatic, smooth and rough endoplasmic reticulum and Golgi), in mitochondrial membranes and in lysosomal membranes. The results indicate that choline deficiency produces oxidative damage in kidney subcellular membranes. Necrosis involved mainly convoluted tubules and appered with a t = 5.5 days. An increase in the production of reactive oxygen species, triggered by NADH overproduction in the mitochondrial dysfunction associated with choline deficiency appears as one of the pathogenic mechanism of mitochondrial and cellular oxidative damage in choline-deficiency.