“…Pups exposed to the P2 protocol presented oxidative damage in the brain, which was verified by the increase in lipid peroxidation, inhibition of -ALA-D activity, marked reduction in non-enzymatic antioxidant parameters (NPSH and ascorbic acid), and inhibition of SOD and catalase activities. These results are in accordance with previous data demonstrating that oxidative stress caused by cigarette smoke exposure causes a decrease in the concentration of some antioxidants (Sobczak et al, 2004;Avti et al, 2006).…”
The protective effect of diphenyl diselenide, (PhSe) 2 , on oxidative stress induced by cigarette smoke exposure in brains of rat pups was evaluated. Animals were exposed to passive cigarette smoke (15 min/day) in two different experimental protocols: P1 (1, 2, and 3 cigarettes) and P2 (4, 5, and 6 cigarettes) for 3 weeks. Before each period of smoke exposure, animals received an oral administration of (PhSe) 2 (0.5 mg/kg). A number of toxicological parameters in the brain were examined, such as lipid peroxidation, δ-aminolevulinate dehydratase (δ-ALA-D) activity, and components of enzymatic (superoxide dismutase and catalase activities) and non-enzymatic antioxidant defenses (ascorbic acid and non-protein thiol levels). In P1, smoke exposure induced an inhibition of catalase activity and an increase of ascorbic acid levels. (PhSe) 2 treatment was able to protect catalase activity but not ascorbic acid levels. In P2, an augmentation of lipid peroxidation, a reduction of enzymatic and non-enzymatic antioxidant status, and an inhibition of δ-ALA-D activity caused by smoke exposure were found. (PhSe) 2 protected the brains of rat pups against oxidative damage induced by smoke exposure. The results are consistent with the antioxidant effect of (PhSe) 2 demonstrated by the reduction of oxidative changes caused by smoke exposure in the brains of pups.
“…Pups exposed to the P2 protocol presented oxidative damage in the brain, which was verified by the increase in lipid peroxidation, inhibition of -ALA-D activity, marked reduction in non-enzymatic antioxidant parameters (NPSH and ascorbic acid), and inhibition of SOD and catalase activities. These results are in accordance with previous data demonstrating that oxidative stress caused by cigarette smoke exposure causes a decrease in the concentration of some antioxidants (Sobczak et al, 2004;Avti et al, 2006).…”
The protective effect of diphenyl diselenide, (PhSe) 2 , on oxidative stress induced by cigarette smoke exposure in brains of rat pups was evaluated. Animals were exposed to passive cigarette smoke (15 min/day) in two different experimental protocols: P1 (1, 2, and 3 cigarettes) and P2 (4, 5, and 6 cigarettes) for 3 weeks. Before each period of smoke exposure, animals received an oral administration of (PhSe) 2 (0.5 mg/kg). A number of toxicological parameters in the brain were examined, such as lipid peroxidation, δ-aminolevulinate dehydratase (δ-ALA-D) activity, and components of enzymatic (superoxide dismutase and catalase activities) and non-enzymatic antioxidant defenses (ascorbic acid and non-protein thiol levels). In P1, smoke exposure induced an inhibition of catalase activity and an increase of ascorbic acid levels. (PhSe) 2 treatment was able to protect catalase activity but not ascorbic acid levels. In P2, an augmentation of lipid peroxidation, a reduction of enzymatic and non-enzymatic antioxidant status, and an inhibition of δ-ALA-D activity caused by smoke exposure were found. (PhSe) 2 protected the brains of rat pups against oxidative damage induced by smoke exposure. The results are consistent with the antioxidant effect of (PhSe) 2 demonstrated by the reduction of oxidative changes caused by smoke exposure in the brains of pups.
“…In fact, the influence of tobacco smoking on the level of α-tocopherol has been well documented, and divergent data exist concerning γ-tocopherol only 33. We believe that the reason for discrepancy between our findings and the results reported in other studies may be related to the assessment of smoking habit based on a questionnaire only and not on more objective methods, such as assessment of the cotinine concentration in urine/plasma.…”
“…28 Cigarette smoking leads to mesangial cell proliferation as well as induction of extracellular matrix proteins and generation of ROS. [13][14][15][16][17][18][19][20][21] The use of calcineurin-free regimens consists of a combination of sirolimus and mycophenolate mofetil, but these agents alone or in combination can result in increased proteinuria in organ transplant recipients. 29 -37 PTE cells are an important component of renal tissue and play a major role in nephron damage.…”
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