Mitochondrial tyrosine nitration precedes chronic allograft nephropathy

MacMillan-Crow, L.A.

doi:10.1016/s0891-5849(01)00750-x

Cited by 92 publications

(55 citation statements)

References 19 publications

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“…Together with recent studies showing tyrosine nitration of mitochondrial proteins in renal allograft rejection (35), our studies support the hypothesis that a variety of mitochondrial proteins are targets of NO in organ rejection. Although our studies do not directly address the potential modification of cytosolic aconitase by NO in this model, it should be recognized that cytosolic aconitase may be important.…”

Section: Discussionsupporting

confidence: 87%

Non-heme iron protein: A potential target of nitric oxide in acute cardiac allograft rejection

Pieper

Halligan

Hilton

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Section: Discussionsupporting

confidence: 87%

Non-heme iron protein: A potential target of nitric oxide in acute cardiac allograft rejection

Pieper

Halligan

Hilton

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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“…Other biologically relevant features of ONOO -include posttranslational tyrosine nitration and consequent modification of protein function (16) as exemplified by mitochondrial manganese O 2 -dismutase (MnSOD), the enzyme that normally keeps concentrations of O 2 -dismutase (SOD) under tight control (17). ONOO --mediated nitration of MnSOD inactivates the enzyme, leading to an increase in O 2 -levels (18)(19)(20)(21)(22), an event favoring increased ONOO -formation, which in turn contributes to the development of hyperalgesia associated with acute inflammation and occurs in response to NMDA receptor activation (14,15). The role(s) and significance of posttranslational nitration in opiate tolerance are currently unknown.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic manipulation of peroxynitrite attenuates the development of opiate-induced antinociceptive tolerance in mice

Muscoli¹,

Cuzzocrea²,

Ndengele³

et al. 2007

J. Clin. Invest.

132

195

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Severe pain syndromes reduce quality of life in patients with inflammatory and neoplastic diseases, often because chronic opiate therapy results in reduced analgesic effectiveness, or tolerance, leading to escalating doses and distressing side effects. The mechanisms leading to tolerance are poorly understood. Our studies revealed that development of antinociceptive tolerance to repeated doses of morphine in mice was consistently associated with the appearance of several tyrosine-nitrated proteins in the dorsal horn of the spinal cord, including the mitochondrial isoform of superoxide (O 2 -) dismutase, the glutamate transporter GLT-1, and the enzyme glutamine synthase. Furthermore, antinociceptive tolerance was associated with increased formation of several proinflammatory cytokines, oxidative DNA damage, and activation of the nuclear factor poly(ADPribose) polymerase. Inhibition of NO synthesis or removal of O 2 -blocked these biochemical changes and inhibited the development of tolerance, pointing to peroxynitrite (ONOO -), the product of the interaction between O 2 -and NO, as a signaling mediator in this setting. Indeed, coadministration of morphine with the ONOO -decomposition catalyst, Fe(III) 5,10,15,20-tetrakis(N-methylpyridinium-4-yl)porphyrin, blocked protein nitration, attenuated the observed biochemical changes, and prevented the development of tolerance in a dose-dependent manner. Collectively, these data suggest a causal role for ONOO -in pathways culminating in antinociceptive tolerance to opiates. Peroxynitrite (ONOO -) decomposition catalysts may have therapeutic potential as adjuncts to opiates in relieving suffering from chronic pain.

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“…Previously, using a rat model of renal I/R [11] and transplantation [26,27] we reported that MnSOD, the major mitochondrial antioxidant, was inactivated before the onset of renal dysfunction, suggesting that loss of mitochondria antioxidant protection might play an important role in I/R related renal injury. MnSOD is the major antioxidant in the mitochondria.…”

Section: Introductionmentioning

confidence: 99%

Manganese porphyrin reduces renal injury and mitochondrial damage during ischemia/reperfusion

Saba

Batinić‐Haberle

Munusamy

et al. 2007

Free Radical Biology and Medicine

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Renal ischemia/reperfusion (I/R) injury often occurs as a result of vascular surgery, organ procurement, or transplantation. We previously showed that renal I/R results in ATP depletion, oxidant production, and manganese superoxide dismutase (MnSOD) inactivation. There have been several reports that overexpression of MnSOD protects tissues/organs from I/R related damage, thus a loss of MnSOD activity during I/R likely contributes to tissue injury. The present study examined the therapeutic benefit of a catalytic antioxidant Mn(III) meso-tetrakis(N-hexylpyridinium-2-yl) porphyrin, (MnTnHex-2-PyP 5+ ) using the rat renal I/R model. This was the first study to examine the effects of MnTnHex-2-PyP 5+ in an animal model of oxidative stress injury. Our results showed that porphyrin pretreatment of rats for 24 hr protected against ATP depletion, MnSOD inactivation, nitrotyrosine formation, and renal dysfunction. The dose (50 μg/kg) used in this study is lower than doses of various types of antioxidants commonly used in animal models of oxidative stress injuries. In addition, using novel proteomic techniques, we identified ATP synthase-beta subunit as a key protein induced by MnTnHex-2-PyP 5+ treatment alone, and complex V (ATP synthase) as a target of injury during renal I/R. These results showed that MnTnHex-2-PyP 5+ protected against renal I/R injury via induction of key mitochondrial proteins that may be capable of blunting oxidative injury.

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Mitochondrial tyrosine nitration precedes chronic allograft nephropathy

Cited by 92 publications

References 19 publications

Non-heme iron protein: A potential target of nitric oxide in acute cardiac allograft rejection

Non-heme iron protein: A potential target of nitric oxide in acute cardiac allograft rejection

Therapeutic manipulation of peroxynitrite attenuates the development of opiate-induced antinociceptive tolerance in mice

Manganese porphyrin reduces renal injury and mitochondrial damage during ischemia/reperfusion

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