RESUMEN
Considering the preexisting influence of the process of natural aging on antioxidant enzymes activity and the level of lipid peroxidation, the age of the rats at which D-galactose (D-gal) treatment is started could strongly impact the development of D-gal induced senescence. To evaluate this, we subjected 1, 3 and 15 months old rats to D-gal treatment in parallel with having appropriate placebos (0.9 % saline). Our results showed elevated glutathione peroxidase (GPx) activity and no significant changes in superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) activity or malondialdehyde (MDA) levels in relation to natural aging. In mature and aged senescent livers we observed positive correlation between increased ratio R=SOD/(GPx+CAT) and increased MDA concentration. MDA levels seemed to correlate positively with the age of the animals at which D-gal treatment had started. In the case of 3 and 15 months old rats there was D-gal induced decrease in SOD and GR activity, but this effect of the treatment was not observed in 1 month old rats. Our results imply that the changes in the antioxidant enzyme activities are not only under the influence of the D-gal overload, but also depend on the developmental stage of the rats. According to our results, with regard to enzymatic antioxidant capacity and the level of lipid peroxidation, the best age for induction of senescence is somewhere after the third month.
Asunto(s)
Envejecimiento/metabolismo , Antioxidantes/metabolismo , Enzimas/metabolismo , Galactosa/farmacología , Riñón/efectos de los fármacos , Hígado/efectos de los fármacos , Factores de Edad , Animales , Biomarcadores/metabolismo , Catalasa/metabolismo , Senescencia Celular/efectos de los fármacos , Femenino , Glutatión Peroxidasa/metabolismo , Glutatión Reductasa/metabolismo , Riñón/enzimología , Peroxidación de Lípido/efectos de los fármacos , Hígado/enzimología , Masculino , Malondialdehído/metabolismo , Ratas Wistar , Factores Sexuales , Superóxido Dismutasa/metabolismoRESUMEN
The aim of this study was to investigate the effect of chronic treatment with chromium hexavalent (Cr VI) on the platelet activation, inflammation and lipid peroxidation in rats. Thirty male Wistar rats weighing 251 ± 18 g were randomly assigned to one control and one Cr-exposed group. 8-iso-prostaglandin F(2α) (8-iso-PGF(2α)), interleukin 1ß (IL-1ß), tumor necrosis factor alpha (TNF-alpha) and creatinine (Crt), were measured in plasma, while 11-dehydro thromboxane B2 (11-dehydro-TXB2) in plasma andurine. Plasma levels of IL-1ß, TNF-alpha, 8-iso-PGF(2α) and Crt were significantly increased in the Cr (VI)-treated in comparison to the control group. Also, in the urine of Cr (VI)-treated rats, 11-dehydro-TXB2 was significantly increased in comparison to control rats. From the obtained data it is evident that chronic treatment with Cr (VI), accelerates arachidonic acid peroxidation in rats, which peroxidation further probably induces enhanced 11-dehydro-TXB2 excretion rate.
Asunto(s)
Cromo/toxicidad , Peroxidación de Lípido/efectos de los fármacos , Activación Plaquetaria/efectos de los fármacos , Animales , Dinoprost/análogos & derivados , Dinoprost/sangre , Dinoprost/orina , Inflamación/sangre , Inflamación/inducido químicamente , Inflamación/orina , Interleucina-1beta/sangre , Masculino , Ratas , Ratas Wistar , Tromboxano B2/análogos & derivados , Tromboxano B2/sangre , Tromboxano B2/orina , Factor de Necrosis Tumoral alfa/sangreRESUMEN
To investigate the role of mitochondrial antioxidant capacity during increased susceptibility to heat accompanied by the aging, young and aged Wistar rats were exposed on heat for 60 min. After heat exposure, hepatic and brain mitochondria were isolated. Our results revealed changes in antioxidant enzyme activities in liver and brain mitochondria from young and to a greater extent in aged rats. Our measurements of MnSOD, GPx and GR activity indicate greater reactive oxygen species production from the mitochondria of aged heat exposed in comparison to young heat exposed rats. Also in the aged rats, the effect of alpha-tocopherol treatment in the prevention of oxidative stress occurred as a result of heat exposure, is less pronounced. Taken together, our data suggest that mitochondria in aged rats are more vulnerable and less able to prevent oxidative changes that occur in response to acute heat exposure.