Protein carbonyl formation and tyrosine nitration as markers of oxidative damage during ischaemia-reperfusion injury to rat sciatic nerve

He, Kai; Nukada, Hitoshi; McMorran, P. Denise; Murphy, Michael P.

doi:10.1016/s0306-4522(99)00350-4

Cited by 44 publications

(24 citation statements)

References 48 publications

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“…Such changes are typical of those seen in nerve tissue after ischemia-reperfusion injury [24] in which ROS formation plays a major role [25]. In fact, diabetic animals are more susceptible to nerve damage as a result of ischemic injury [10, 11], though typically the mechanism of ischemia in animal models is acute and severe (e.g., temporary ligation of major arteries in the hindlimb).…”

Section: Discussionmentioning

confidence: 99%

Cold Exposure Exacerbates the Development of Diabetic Polyneuropathy in the Rat

Kasselman

Veves

Gibbons

et al. 2009

Experimental Diabetes Research

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Diabetic polyneuropathy (DPN) and cold-induced nerve injury share several pathogenic mechanisms. This study explores whether cold exposure contributes to the development of DPN. Streptozotocin-induced diabetic rats and controls were exposed to a room temperature (23°C) or cold environment (10°C). H-reflex, tail and sciatic motor, and sensory nerve conduction studies were performed. Analyses of sural nerve, intraepidermal nerve fibers, and skin and nerve nitrotyrosine ELISAs were performed. Diabetic animals exposed to a cold environment had an increased H-reflex four weeks earlier than diabetic room temperature animals (P = .03). Cold-exposed diabetic animals also had greater reduction in motor conduction velocities at 20 weeks (P = .017), decreased skin nerve fiber density (P = .037), and increased skin nitrotyrosine levels (P = .047). Cold exposure appears to hasten the development of DPN in the rat STZ model of diabetes. These findings support that further study into the relationship between ambient temperature and DPN is warranted.

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Section: Discussionmentioning

confidence: 99%

Cold Exposure Exacerbates the Development of Diabetic Polyneuropathy in the Rat

Kasselman

Veves

Gibbons

et al. 2009

Experimental Diabetes Research

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“…Mild additional ischemia, insufficient to cause fiber degeneration in normal nerves, will regularly cause fiber degeneration in EDN [4][5][6]. In this model, there is prominent fiber degeneration associated with oxidative injury and an inflammatory response [2,7,8]. This vulnerability is reported to be fully developed by 4 months but is absent at 2 weeks [6].…”

Section: Introductionmentioning

confidence: 87%

Ischemia–reperfusion injury of peripheral nerve in experimental diabetic neuropathy

Wang

Schmelzer

Schmeichel

et al. 2004

Journal of the Neurological Sciences

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“…Addition of antioxidant selenium resulted in prevention of formation of 3-nitrotyrosine, 24 h after incubation of PC12 cell cultures with methamphetamine, which caused significant formation of 3-nitrotyrosine, a marker of peroxynitrite generation (Imam & Ali, 2000). An increase in the concentration of 3-nitrotyrosine has been implicated in various diseases that resulted in oxidative stress conditions (Gole et al, 2000;He et al, 1999;Lamb et al, 1999;Oats et al, 1999;Tohgi et al, 1999b). Kato et al (2000) showed a significant correlation between expression of 3-nitrotyrosine in carcinoma cells and the depth of tumor invasion.…”

Section: -Nitrotyrosinementioning

confidence: 92%

BIOMARKERS OF APOPTOSIS: RELEASE OF CYTOCHROME c, ACTIVATION OF CASPASE-3, INDUCTION OF 8-HYDROXY-2'-DEOXYGUANOSINE, INCREASED 3-NITROTYROSINE, AND ALTERATION OF p53 GENE

Abu-Qare¹,

Abou‐Donia²

2001

Journal of Toxicology and Environmental Health Part B: Critical Reviews

160

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Biomarkers rely on biochemical, histological, morphological, and physiological changes in whole organisms. Their use is becoming an important tool to examine changes at cellular and molecular levels, especially in nucleic acids and proteins. Biomarkers are used to measure exposure to a toxic agent, to detect severity of any toxic response, and to predict the possible outcome. Information on the mechanisms of action of toxicants can allow the development of potential biomarkers of effect and thus improvement of the risk assessment processes. Use of biomarkers as a tool to predict induction of apoptosis allows identification of biological signs that may indicate increased risk for disease. In cells undergoing apoptosis, the release of cytochrome c from the mitochondria to the cytoplasm and the activation of caspase-3, a key enzyme to execution stage of apoptotic pathway, have been studied as biomarkers of cell death (apoptosis). Products of DNA fragmentation that either accumulate in the cellular tissues or are excreted in the urine are useful markers of DNA damage. The induction level of urinary or cellular level of 8-hydroxy-2-deoxyguanosine and 3-nitrotyrosine has been used as a marker to measure extent of DNA oxidative damage. Furthermore, alteration or overexpression of the p53 gene was considered an indication of apoptosis. This article reviews some of the aspects of biomarkers of apoptosis, indicating relevance of their uses to predict apoptosis following exposure to environmental toxicants.

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Protein carbonyl formation and tyrosine nitration as markers of oxidative damage during ischaemia-reperfusion injury to rat sciatic nerve

Cited by 44 publications

References 48 publications

Cold Exposure Exacerbates the Development of Diabetic Polyneuropathy in the Rat

Cold Exposure Exacerbates the Development of Diabetic Polyneuropathy in the Rat

Ischemia–reperfusion injury of peripheral nerve in experimental diabetic neuropathy

BIOMARKERS OF APOPTOSIS: RELEASE OF CYTOCHROME c, ACTIVATION OF CASPASE-3, INDUCTION OF 8-HYDROXY-2'-DEOXYGUANOSINE, INCREASED 3-NITROTYROSINE, AND ALTERATION OF p53 GENE

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