Increased oxidative stress is correlated with mitochondrial dysfunction in chagasic patients

Wen, Julie; Yachelini, Pedro; Sembaj, Adela; Manzur, Rafael E.; Garg, Nisha

doi:10.1016/j.freeradbiomed.2006.04.009

Cited by 110 publications

(112 citation statements)

References 34 publications

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“…We have monitored MDA levels, an LPO product, and a marker of oxidative damage by TBARS assay. MDA is a reflection of the extent of oxidant status and is considered a good marker of oxidative stress (Wen et al 2006).…”

Section: Assessment Of Insulin Actionmentioning

confidence: 99%

Hyperglycemia induces apoptosis in rat liver through the increase of hydroxyl radical: new insights into the insulin effect

Francés

Ronco²,

Monti³

et al. 2010

Journal of Endocrinology

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In this study, we analyzed the contribution of hydroxyl radical in the liver apoptosis mediated by hyperglycemia through the Bax-caspase pathway and the effects of insulin protection against the apoptosis induced by hyperglycemia. Male adult Wistar rats were randomized in three groups: control (C) (sodium citrate buffer, i.p.), streptozotocin (STZ)-induced diabetic (SID) (STZ 60 mg/kg body weight, i.p.), and insulintreated SID (SIDCI; 15 days post STZ injection, SID received insulin s.c., twice a day, 15 days). Rats were autopsied on day 30. In liver tissue, diabetes promoted a significant increase in hydroxyl radical production which correlated with lipid peroxidation (LPO) levels. Besides, hyperglycemia significantly increased mitochondrial BAX protein expression, cytosolic cytochrome c levels, and caspase-3 activity leading to an increase in apoptotic index. Interestingly, the treatment of diabetic rats with desferoxamine or tempol (antioxidants/ hydroxyl radical scavengers) significantly attenuated the increase in both hydroxyl radical production and in LPO produced by hyperglycemia, preventing apoptosis by reduction of mitochondrial BAX and cytosolic cytochrome c levels. Insulin treatment showed similar results. The finding that co-administration of antioxidants/hydroxyl radical scavengers together with insulin did not provide any additional benefit compared with those obtained using either inhibitors or insulin alone shows that it is likely that insulin prevents oxidative stress by reducing the effects of hydroxyl radicals. Importantly, insulin significantly increased apoptosis inhibitor protein expression by induction of its mRNA. Taken together, our studies support that, at least in part, the hydroxyl radical acts as a reactive intermediate, which leads to liver apoptosis in a model of STZ-mediated hyperglycemia. A new anti-apoptosis signal for insulin is shown, given by an increase of apoptosis inhibitor protein.

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Section: Assessment Of Insulin Actionmentioning

confidence: 99%

Hyperglycemia induces apoptosis in rat liver through the increase of hydroxyl radical: new insights into the insulin effect

Francés

Ronco²,

Monti³

et al. 2010

Journal of Endocrinology

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“…As myocarditis progresses, a substantial decline in cardiac mtDNA content (54-60%) and mitochondria-encoded transcripts (50-65%) indicate that alterations in mtDNA contribute to the quantitative deficiencies in respiratory chain activity of infected individuals (Vyatkina et al 2004). In fact, during chagasic cardiomyopathy, mitochondrial dysfunction occurs as a consequence of intense oxidative stress (Wen et al 2006) and is evidenced by deficiencies in respiratory chain complexes (CI-CV) (Garg 2005).…”

Section: The Dual Role Of No During T Cruzi Infectionmentioning

confidence: 99%

The effects of nitric oxide on the immune system during Trypanosoma cruzi infection

Gutierrez

Mineo

Pavanelli

et al. 2009

Mem. Inst. Oswaldo Cruz

109

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“…In previous studies, our and other groups have provided evidence showing that Chagas disease causes the disruption of heart and cardiomyocyte function, primarily due to a sustained inflammatory response, leading to nitric oxide and superoxide anion production (de Carvalho et al 1992, Machado et al 2000, Wen et al 2006, Macao et al 2007, Sales et al 2008, RomanCampos et al 2009a. Additionally, it is accepted that sustained and excessive superoxide production is able to downregulate heart and cardiomyocyte function, mainly through the disruption of excitation-contraction coupling (Prosser et al 2011) and reduction of Kv4.3 expression (Zhou et al 2006).…”

mentioning

confidence: 93%

Cardiomyocyte dysfunction during the chronic phase of Chagas disease

Roman‐Campos¹,

Sales-Junior

Duarte³

et al. 2013

Mem. Inst. Oswaldo Cruz

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Increased oxidative stress is correlated with mitochondrial dysfunction in chagasic patients

Cited by 110 publications

References 34 publications

Hyperglycemia induces apoptosis in rat liver through the increase of hydroxyl radical: new insights into the insulin effect

Hyperglycemia induces apoptosis in rat liver through the increase of hydroxyl radical: new insights into the insulin effect

The effects of nitric oxide on the immune system during Trypanosoma cruzi infection

Cardiomyocyte dysfunction during the chronic phase of Chagas disease

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