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Scavenging reactive oxygen species using tempol in the acute phase of renal ischemia/reperfusion and its effects on kidney oxygenation and nitric oxide levels.

Aksu U, Ergin B, Bezemer R, Kandil A, Milstein DM, Demirci-Tansel C, Ince C - Intensive Care Med Exp (2015)

Bottom Line: I/R was induced by 30-min clamping of the renal artery.At R90, the creatinine clearance rate was lower in the I/R-subjected group that did not receive tempol compared to that in the other groups.Tempol administration before I/R could prevent oxidative stress and altered tissue NO levels.

View Article: PubMed Central - PubMed

Affiliation: Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands, uguraksu@istanbul.edu.tr.

ABSTRACT

Background: Renal ischemia/reperfusion (I/R) injury is commonly seen in kidney transplantation and affects the allograft survival rates. We aimed to test our hypothesis that scavenging reactive oxygen species (ROS) with tempol would protect renal oxygenation and nitric oxide (NO) levels in the acute phase of renal I/R.

Methods: Rats were randomly divided: (1) no I/R, no tempol; (2) no I/R, but with tempol; (3) I/R without tempol; and (4) I/R with tempol. I/R was induced by 30-min clamping of the renal artery. Tempol (200 μmol/kg/h/i.v) was administered 15 min prior to I/R.

Results: I/R without tempol led to a significant decrease in renal oxygen delivery and microvascular oxygenation. Tempol, however, protected renal oxygenation after I/R. At R90, the creatinine clearance rate was lower in the I/R-subjected group that did not receive tempol compared to that in the other groups. I/R injury without tempol treatment led to a significant increase in tissue malondialdehyde levels and a significant decrease in tissue NO levels. Tempol administration before I/R could prevent oxidative stress and altered tissue NO levels.

Conclusions: This underscores that unbalance between oxygen, NO, and ROS forms an important component of the pathogenesis of I/R-induced AKI and should therefore be taken into account when designing a prevention/treatment strategy for renal I/R injury in transplantation.

No MeSH data available.


Related in: MedlinePlus

Renal oxygenation, oxidative stress, and nitric oxide (NO) levels at the end of the protocol. a Microvascular oxygen tensions (μpO2) in the renal cortex; b Microvascular oxygen tensions (μpO2) in the renal medulla; c renal tissue malondialdehyde (MDA) levels normalized to the tissue protein content; and d tissue NO levels normalized to the tissue protein content. *p < 0.05 vs all other groups; Cp < 0.05 vs the CTRL group; Tp < 0.05 vs the TMPL group
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Fig1: Renal oxygenation, oxidative stress, and nitric oxide (NO) levels at the end of the protocol. a Microvascular oxygen tensions (μpO2) in the renal cortex; b Microvascular oxygen tensions (μpO2) in the renal medulla; c renal tissue malondialdehyde (MDA) levels normalized to the tissue protein content; and d tissue NO levels normalized to the tissue protein content. *p < 0.05 vs all other groups; Cp < 0.05 vs the CTRL group; Tp < 0.05 vs the TMPL group

Mentions: The renal microvascular oxygenation, oxidative stress, and NO levels at the end of the protocol are presented in Fig. 1. Tempol administration without I/R injury led to a significant decrease in tissue MDA levels (1.6 ± 0.17) and I/R injury in the absence of tempol led to a significant increase in tissue MDA levels (3.8 ± 0.9). Tempol administration before I/R could partially prevent this increase in MDA levels (2.4 ± 0.7). Tissue NO levels were not affected by tempol administration without I/R injury (240 ± 100), but were significantly decreased after I/R in the absence of tempol (72 ± 21). Tempol administration before I/R could completely normalize the tissue NO levels (265 ± 143). Hence, tempol administration prior to I/R injury reduced renal oxidative stress and normalized renal oxygenation and tissue NO levels.Fig. 1


Scavenging reactive oxygen species using tempol in the acute phase of renal ischemia/reperfusion and its effects on kidney oxygenation and nitric oxide levels.

Aksu U, Ergin B, Bezemer R, Kandil A, Milstein DM, Demirci-Tansel C, Ince C - Intensive Care Med Exp (2015)

Renal oxygenation, oxidative stress, and nitric oxide (NO) levels at the end of the protocol. a Microvascular oxygen tensions (μpO2) in the renal cortex; b Microvascular oxygen tensions (μpO2) in the renal medulla; c renal tissue malondialdehyde (MDA) levels normalized to the tissue protein content; and d tissue NO levels normalized to the tissue protein content. *p < 0.05 vs all other groups; Cp < 0.05 vs the CTRL group; Tp < 0.05 vs the TMPL group
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4491093&req=5

Fig1: Renal oxygenation, oxidative stress, and nitric oxide (NO) levels at the end of the protocol. a Microvascular oxygen tensions (μpO2) in the renal cortex; b Microvascular oxygen tensions (μpO2) in the renal medulla; c renal tissue malondialdehyde (MDA) levels normalized to the tissue protein content; and d tissue NO levels normalized to the tissue protein content. *p < 0.05 vs all other groups; Cp < 0.05 vs the CTRL group; Tp < 0.05 vs the TMPL group
Mentions: The renal microvascular oxygenation, oxidative stress, and NO levels at the end of the protocol are presented in Fig. 1. Tempol administration without I/R injury led to a significant decrease in tissue MDA levels (1.6 ± 0.17) and I/R injury in the absence of tempol led to a significant increase in tissue MDA levels (3.8 ± 0.9). Tempol administration before I/R could partially prevent this increase in MDA levels (2.4 ± 0.7). Tissue NO levels were not affected by tempol administration without I/R injury (240 ± 100), but were significantly decreased after I/R in the absence of tempol (72 ± 21). Tempol administration before I/R could completely normalize the tissue NO levels (265 ± 143). Hence, tempol administration prior to I/R injury reduced renal oxidative stress and normalized renal oxygenation and tissue NO levels.Fig. 1

Bottom Line: I/R was induced by 30-min clamping of the renal artery.At R90, the creatinine clearance rate was lower in the I/R-subjected group that did not receive tempol compared to that in the other groups.Tempol administration before I/R could prevent oxidative stress and altered tissue NO levels.

View Article: PubMed Central - PubMed

Affiliation: Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands, uguraksu@istanbul.edu.tr.

ABSTRACT

Background: Renal ischemia/reperfusion (I/R) injury is commonly seen in kidney transplantation and affects the allograft survival rates. We aimed to test our hypothesis that scavenging reactive oxygen species (ROS) with tempol would protect renal oxygenation and nitric oxide (NO) levels in the acute phase of renal I/R.

Methods: Rats were randomly divided: (1) no I/R, no tempol; (2) no I/R, but with tempol; (3) I/R without tempol; and (4) I/R with tempol. I/R was induced by 30-min clamping of the renal artery. Tempol (200 μmol/kg/h/i.v) was administered 15 min prior to I/R.

Results: I/R without tempol led to a significant decrease in renal oxygen delivery and microvascular oxygenation. Tempol, however, protected renal oxygenation after I/R. At R90, the creatinine clearance rate was lower in the I/R-subjected group that did not receive tempol compared to that in the other groups. I/R injury without tempol treatment led to a significant increase in tissue malondialdehyde levels and a significant decrease in tissue NO levels. Tempol administration before I/R could prevent oxidative stress and altered tissue NO levels.

Conclusions: This underscores that unbalance between oxygen, NO, and ROS forms an important component of the pathogenesis of I/R-induced AKI and should therefore be taken into account when designing a prevention/treatment strategy for renal I/R injury in transplantation.

No MeSH data available.


Related in: MedlinePlus