Exogenous ATP administration prevents ischemia/reperfusion-induced oxidative stress and tissue injury by modulation of hypoxanthine metabolic pathway in rat ovary

Kumbasar, Serkan; Cetin, Nihal; Yapça, Ömer Erkan; Şener, Ebru; İsaoğlu, Ünal; Yilmaz, ehmet; Salman, Süleyman; Aksoy, Ayşe Nur; Gül, Mehmet; Süleyman, Halis

doi:10.1590/0103-8478cr20131006

Cited by 10 publications

(8 citation statements)

References 25 publications

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“…35 Additionally, Kumbasar et al reported that the severity of the histopathological findings observed in ovarian IR injury were parallel to an increase of xanthine oxidase metabolism products (oxidants). 36 Kineret® inhibited this histopathological damage at a dose of 100 mg/kg more effectively when compared to a dose of 50 mg/kg. Moreover, Kineret® has been reported to protect tissues from oxidative damage by inhibiting IL-β gene expression.…”

Section: Discussionmentioning

confidence: 90%

Effect of Kineret® on ovarian ischemia reperfusion injury in a rat model

Naykı

Cetin

et al. 2016

J of Obstet and Gynaecol

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Section: Discussionmentioning

confidence: 90%

Effect of Kineret® on ovarian ischemia reperfusion injury in a rat model

Naykı

Cetin

et al. 2016

J of Obstet and Gynaecol

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“…This dose was shown to protect ovarian tissue from oxidative ischemia reperfusion injury in a previous study. 39 Same volume normal saline (0.9% NaCl) as solvent was administered ip to the other two groups including SG (n ¼ 10) and HG (n ¼ 10). After 1 h from administration of ATP and 0.9% NaCI, 25 mg/kg sunitinib was applied orally via catheter to stomach in the SAG and SG groups.…”

Section: Experiments Proceduresmentioning

confidence: 99%

The effect of adenosine triphosphate on sunitinib-induced cardiac injury in rats

et al. 2020

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In this study, we aimed to show the effect of adenosine 5′-triphosphate (ATP) on sunitinib-induced cardiac injury in rats. The rats ( n = 30) were divided equally into three groups as sunitinib group (SG), sunitinib plus ATP group (SAG), and healthy group (HG); 2 mg/kg ATP was injected intraperitoneally (ip) to the SAG group. Same volume normal saline as solvent was administered ip to the other two groups. After 1 h, 25 mg/kg sunitinib was applied orally via catheter to stomach in the SAG and SG groups. This procedure was repeated once daily for 5 weeks. At the end of this period, all animals were sacrificed and their cardiac tissue was removed. Malondialdehyde (MDA), total glutathione (tGSH), tumor necrosis factor α (TNF- α), and nuclear factor κB (NF- κB) levels in rats’ cardiac tissues and troponin I (Tp-I) levels in rats’ blood samples were evaluated. Histopathological analysis was also performed in cardiac tissues of the animals. MDA, TNF- α, NF- κB, and Tp-I levels were higher in the SG group compared to the SAG and HG groups ( p < 0.001). tGSH levels of the SG group were lower than the SAG and HG groups ( p < 0.001). The structure and morphology of cardiac muscle fibers and blood vessels were normal in the control group. In the SG group, obvious cardiac muscle tissue damage with dilated myofibers, locally atrophic myofibers, and congested blood vessels were observed. In the SAG group, marked amelioration in these findings was observed. We showed this for the first time that ATP administration exerts a protective effect against cardiac effects of sunitinib.

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“…Kumbasar et al [ 22 ] reported that externally provided ATP protected ischemic tissue from oxidative stress by inhibiting the overproduction of xanthine oxidase and MDA, and consumption of tGSH. However, the information on whether ATP could enter or exit the cell was not well known until a certain time.…”

Section: Discussionmentioning

confidence: 99%

“…The energy released from ATP degradation is the primary energy source for muscle contraction [ 21 ]. Kumbasar et al [ 22 ] have highlighted that exogenous ATP protects ischemic tissue from oxidative stress by inhibiting the excessive production of oxidant markers such as xanthine oxidase and malondialdehyde and the consumption of antioxidant total glutathione. It is understood from the literature that rhabdomyolysis is a clinical condition of skeletal muscle destruction.…”

Section: Introductionmentioning

confidence: 99%