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Vol.4 , No. 1, Publication Date: Sep. 26, 2017, Page: 1-7
 of a genetically obese rat. Ten adult male rats were distributed into Zucker (fa-/fa-, n=5) and lean Zucker (fa+/fa-, n=5). Osmotic swelling, reactive oxygen species (ROS), oxidation of thiols and reduced glutathione (GSH) were measured in of renal and hepatic tissues of lean and Zucker rats. The kidney mitochondrial swelling was increased in the obese vs. lean in all concentrations, but it was significant only in Ca<sup>+2</sup> (10, 25 or 50 µM); the same was observed in the liver mitochondrial swelling. ROS were significantly increased in liver mitochondria of obese vs. lean, but with no significance statistical in kidney mitochondria. Thiols levels in liver and kidney mitochondrial and homogenate of obese rats did not show statistical differences vs. lean, except in liver homogenate. Obese presented significant reduction of mitochondrial and homogenate GSH levels in kidney and liver vs. lean. These findings demonstrated that obese had higher thiols and ROS and, lower GSH levels, which contributed to mitochondrial dysfunction significant in kidney and liver vs. lean rats. Mitochondrial oxidative stress between obese and lean rats showed difference only in liver; however, the antioxidant system was lower in obese than lean in both, kidney and liver. The results showed that obesity promotes redox imbalance, contributing to mitochondrial dysfunction in both, kidney and liver, being the liver more susceptible than kidney to mitochondria permeabilization, which can be linked to cell death and injury in tissue-specific mitochondrial obesity.&picture=http://www.aascit.org/aascit/decorators/img/journal/972.jpg)
| [1] | André Soares Trindade, Translational Medicine, Universidade Federal de Sao Paulo, Sao Paulo, Brazil. |
| [2] | Priscila Afonso Faria, Center of Natural Sciences and Humanities, Universidade Federal do ABC, Sao Paulo, Brazil. |
| [3] | Marcos Antônio Nascimento, Physical Education Section, Brazilian Air Force (FAB), Sao Paulo, Brazil. |
| [4] | Giovana Rita Punaro, Nephrology Division, Universidade Federal de Sao Paulo, Sao Paulo, Brazil. |
| [5] | Tiago Rodrigues, Center of Natural Sciences and Humanities, Universidade Federal do ABC, Sao Paulo, Brazil. |
| [6] | Marcelo Macedo Rogero, Department of Nutrition, Public Health College, Universidade de Sao Paulo, Sao Paulo, Brazil. |
| [7] | Elisa Mieko Suemitsu Higa, Translational Medicine, Universidade Federal de Sao Paulo, Sao Paulo, Brazil; Nephrology Division, Universidade Federal de Sao Paulo, Sao Paulo, Brazil. |
The aim of this study was to evaluate the redox status and mitochondrial function in renal and hepatic tissues (homogenate and isolated mitochondria) of a genetically obese rat. Ten adult male rats were distributed into Zucker (fa-/fa-, n=5) and lean Zucker (fa+/fa-, n=5). Osmotic swelling, reactive oxygen species (ROS), oxidation of thiols and reduced glutathione (GSH) were measured in of renal and hepatic tissues of lean and Zucker rats. The kidney mitochondrial swelling was increased in the obese vs. lean in all concentrations, but it was significant only in Ca+2 (10, 25 or 50 µM); the same was observed in the liver mitochondrial swelling. ROS were significantly increased in liver mitochondria of obese vs. lean, but with no significance statistical in kidney mitochondria. Thiols levels in liver and kidney mitochondrial and homogenate of obese rats did not show statistical differences vs. lean, except in liver homogenate. Obese presented significant reduction of mitochondrial and homogenate GSH levels in kidney and liver vs. lean. These findings demonstrated that obese had higher thiols and ROS and, lower GSH levels, which contributed to mitochondrial dysfunction significant in kidney and liver vs. lean rats. Mitochondrial oxidative stress between obese and lean rats showed difference only in liver; however, the antioxidant system was lower in obese than lean in both, kidney and liver. The results showed that obesity promotes redox imbalance, contributing to mitochondrial dysfunction in both, kidney and liver, being the liver more susceptible than kidney to mitochondria permeabilization, which can be linked to cell death and injury in tissue-specific mitochondrial obesity.
Keywords
Mitochondria, ROS, Genetic Obese Rats, Liver, Kidney
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