Impaired erythrocytes deformability in H2O2-induced oxidative stress: Protective effect of L-carnosine

Abstract

Impaired red blood cell deformability is a hemorheological perturbation induced by many kinds of diseases. An increase in free radicals causes a reduction in erythrocyte flexibility and deformability. Carnosine is a dipeptide abundant in skeletal muscle and brain of humans. One of the main function of carnosine is its antioxidant and free-radical scavenger effect. In this study our aim is to investigate the protective effect of L-carnosine on RBCs in H 2 O 2 -induced oxidative stress in vitro conditions.Twenty male wistar albino rats, 10 were 3 months old, 10 were 12 months old used. The blood from each rat were divided into ten tubes and these blood samples divided into two groups. The first tube of the first group was the control and the rest 4 tubes were treated with different concentrations of L-carnosine. All tubes in the second group were incubated with H 2 O 2 additively. The deformability indexes of the erythrocytes were measured by a laser diffractometer (Myrenne Rheodyne SSD).L-carnosine has improved the RBC deformability significantly which is impaired by H 2 O 2 treatment (p < 0.05). Increase in deformability is more significant in young rat group when compared to old rat group.L-carnosine, as an antioxidant molecules, has a dose dependent positive effect on RBC deformability and has improved or protect the deformability of erythrocytes, especially in young rat group which impaired by H 2 O 2 -induced oxidative stress in vitro conditions. The results of this study first suggest that L-carnosine supplemention can be used to improve the RBC quality or to protect them from oxidative damage in survival of RBC in the circulation.

Aged garlic extract protects against oxidative stress and renal changes in cisplatin-treated adult male rats

“…The elevation in the kidney biomarkers was due to the direct toxic effect of CP on the glomerular and tubular structures through the generation of ROS. Contraction of the mesangial cells with subsequent alteration in the filtration surface area resulted from the generation of ROS [ 32 ].…”

Antioxidant Effect of Silymarin on Cisplatin-Induced Renal Oxidative Stress in Rats

“…The escalation in the serum levels of these renal functional markers might be caused by the direct toxic effect of CDDP that resulted in: impaired renal functions (Anusuya et al, 2013), glomerular injury, tubular obstruction and/or the back-leakage of the renal tubules (Azu et al, 2010). The alterations in glomerular function in CDDP-treated rats may also be secondary to ROS (Somani et al, 2000) which provoke mesangial cells contraction, modifying the filtration surface area and altering the ultrafiltration coefficient factors that decrease the glomerular filtration rate (Aydogan et al, 2008). Such ROS might play a role in the pathogenesis of tubular cell apoptosis but probably had no effect in the tubular necrosis.…”

Amelioration of cisplatin-induced nephrotoxicity by grape seed extract and fish oil is mediated by lowering oxidative stress and DNA damage

“…In the present study, the observed nephrotoxicity due to cisplatin treatment was manifested by marked increases in serum creatinine, urea and uric acid accompanied by a decrease in urine creatinine, urea, uric acid and creatinine clearance. This may be due to the decrease in the glomerular filtration rate or may be secondary due to the increase of the reactive oxygen species (Noori and Mahboob 2010) which induce mesangial cells contraction, altering the filteration surface area and modifying the ultrafiltration coefficient factors that thereby decrease the glomerular filtration rate (Aydogan et al 2008). These results are in accordance with previous studies (Fouad et al 2008).…”