Nitric oxide and asymmetric dimethyl arginine (ADMA) levels in an experimental hydronephrotic kidney caused by unilateral partial ureteral obstruction

ABSTRACT Aim Our aim is to measure asymmetric dimethyl arginine and nitric oxide levels in rats with induced unilateral acute ureteral obstruction to research the effects on the kidney. Material and Methods The study included 21 adolescent (average age 6 weeks) Sprague-Dawley male rats weighing between 240-290g divided at random into 3 groups. Group-1: Control group (n=6): underwent no procedures. Group-2: Sham group (n=6): underwent the same procedures as the experimental group without ureter and psoas muscle dissection. Group-3: Group with induced partial unilateral ureteral obstruction (n=9). All rats were sacrificed after 12 weeks. Superoxide dismutase enzyme activity and nitrite and nitrate salt levels were measured in renal tissue. Plasma nitrite-nitrate and ADMA levels were examined. Results In the experimental group histopathological changes observed included renal pelvis dilatation, flattened papillae, sclerotic glomerulus and fibrosis. In the experimental group tissue SOD and blood ADMA levels were higher than the control and sham groups (p<0.05) while tissue NO and plasma NO values were lower than in the sham and control groups (p<0.05). Conclusion Oxidative stress and disruption of NO synthesis play an important role in renal function and histopathological changes after obstructive renal disease. To prevent renal complications developing after obstructive nephropathy we believe that a new strategy may be research on reducing ADMA.

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats

To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. The MDA and MPO levels increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P<0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05).The number of apoptotic neurons increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.