Retraction：Dietary Supplementation of L-Carnosine Prevents Ischemia/Reperfusion-Induced Renal Injury in Rats

Fujii, Toshihide; Takaoka, Masanori; Tsuruoka, Nobuo; Kiso, Yoshinobu; Tanaka, Takaharu; Matsumura, Yasuo

doi:10.1248/bpb.28.361

Cited by 34 publications

(15 citation statements)

References 18 publications

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“…16) In addition, dietary supplementation of carnosine attenuated the ischemia /reperfusion-induced renal dysfunction. 17) Hence, ourˆndings suggest that carnosine and captopril may be synergistic antioxidants, and could thus pose less danger of overdose in the inhibition of ACE activity. Deleterious interactions between medicines and food ingredients, including so-called health foods and functional foods, are currently increasing.…”

mentioning

confidence: 73%

Interactions between Carnosine and Captopril on Free Radical Scavenging Activity and Angiotensin-converting Enzyme Activity in vitro

2006

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Interactions between carnosine (b-alanyl-L-histidine), being plentiful in skeletal muscles and neuronal tissues, and captopril, a widely used angiotensin-converting enzyme (ACE) inhibitor, were examined concerning free radical scavenging activity and ACE activity in vitro. Not only captopril, but also carnosine, at concentrations less than those ordinarily found in muscles and neuronal tissues, signiˆcantly scavenged 2,2′ -azinobis(3-ethylbenzothiazoline-6-sulphonate) (ABTS) radical cations, and inhibited ACE activity. Cupric ions reversed the ABTS scavenging activity of carnosine and captopril, whereas cupric ions strengthened the inhibitory action of carnosine on ACE activity. In contrast, cupric ions antagonized the inhibition of ACE activity induced by ethylenediaminetetraacetic acid, indicating that the inhibitory eŠect of carnosine on ACE activity is not related to the chelating action of carnosine. On the other hand, carnosine and captopril synergistically enhanced the free radical scavenging activity, but not the inhibitory eŠect on the ACE activity. These data suggest that carnosine in its concurrent use with captopril could act as a beneˆcial free radical scavenger, with less danger of overdose, in the inhibition of ACE activity.

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confidence: 73%

Interactions between Carnosine and Captopril on Free Radical Scavenging Activity and Angiotensin-converting Enzyme Activity in vitro

2006

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“…19 Carnosine has been reported to play a protective action against ischemic injury. 20,21 So the effect of carnosine on mast cell injury induced by OGD was subsequently investigated.…”

Section: Resultsmentioning

confidence: 99%

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Shen

Zhang

et al. 2007

Cell Biochemistry & Function

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Carnosine (beta-alanyl-histidine) is a naturally occurring dipeptide that has been characterized as a putative hydrophilic antioxidant. The protective function of carnosine has been demonstrated in neuronal cells under ischemic injury. The purpose of this study was to investigate the effects of carnosine on oxygen-glucose deprivation (OGD)-induced degranulation and histamine release from mast cells. Cultured mast cells were exposed to OGD for 4 h, and then the degranulation was observed immediately by microscopy. Histamine release was analyzed by high-performance liquid chromatography (HPLC). OGD caused degranulation of mast cells, and increased histamine and lactate dehydrogenase (LDH) release. Carnosine (at a concentration of 5 mM) alone did not produce any appreciable effect on degranulation, histamine, and LDH release from mast cells under normal condition, but significantly inhibited the degranulation, histamine, and LDH release of mast cells induced by OGD. These results indicate that carnosine can protect mast cells from degranulation and histamine release and it may be an endogenous mast cell stabilizer in the pathological processes induced by ischemia.

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“…The naturally-occurring peptide carnosine (b-alanyl-L-histidine) has been shown to protect against ischemia in a number of animal tissues including brain (Tang et al 2007;Rajanikant et al 2007;Dobrota et al 2005;Min et al 2008), kidney (Fujii et al 2005;Kurata et al 2006), and liver (Baykara et al 2009;Fouad et al 2007), sometimes when the dipeptide was added after the ischemic event (Dobrota et al 2005). Carnosine also delays senescence in cultured human fibroblasts (McFarland and Holliday 1994), possibly due to decreased generation of glycoxidized proteins (Alhamdani et al 2007).…”

Section: Carnosine Glyoxalase Mg and Glycationmentioning

confidence: 99%

NAD+ Availability and Proteotoxicity

Hipkiss

2009

Neuromol Med

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It has been shown that NAD(+) availability is important for neuronal survival following ischemia (Liu et al., Neuromolecular Med 11:28-42, 2009). It is proposed here that NAD(+) may also control proteotoxicity by influencing both formation and catabolism of altered proteins. It is suggested that low NAD(+) availability promotes synthesis of methylglyoxal (MG) which can induce formation of glycated proteins, ROS, and dysfunctional mitochondria. That glyoxalase overexpression and carnosine are both protective against MG and ischemic injury support this proposal. Recognition and elimination of altered proteins is enhanced by NAD(+) through effects on stress protein expression and autophagy.

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Retraction：Dietary Supplementation of L-Carnosine Prevents Ischemia/Reperfusion-Induced Renal Injury in Rats

Cited by 34 publications

References 18 publications

Interactions between Carnosine and Captopril on Free Radical Scavenging Activity and Angiotensin-converting Enzyme Activity in vitro

Interactions between Carnosine and Captopril on Free Radical Scavenging Activity and Angiotensin-converting Enzyme Activity in vitro

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

NAD+ Availability and Proteotoxicity

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