Elucidation of the effects of lipoperoxidation on the mitochondrial electron transport chain using yeast mitochondria with manipulated fatty acid content

Cortés‐Rojo, Christian; Calderón-Cortés, Elizabeth; Clemente‐Guerrero, Mónica; Estrada-Villagomez, M. Mirella; Manzo‐Ávalos, Salvador; Mejía-Zepeda, Ricardo; Boldogh, István; Saavedra‐Molina, Alfredo

doi:10.1007/s10863-009-9200-3

Cited by 37 publications

(31 citation statements)

References 55 publications

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“…In this regard, it is well known that cardiolipin is essential for the activity of a myriad of proteins embedded in mitochondrial membranes, including all the ETC complexes (Chicco and Sparagna 2007). By this reason, lipid peroxidation has an inhibitory role in all the ETC complexes (Forsmark-Andrée et al 1997;Cortés-Rojo et al 2009). Thus, the lack of inhibitory effects by diabetes on the activity of the complexes II and IV, along with the weak, nonstatistically decline in complex III activity, argues against the idea about a central participation of lipid peroxidation in the effects of diabetes on the ETC.…”

Section: Discussionmentioning

confidence: 99%

“…No changes in absorbance were detected in the absence of NADH. The activities of succinate-DCIP oxidoreductase (complex II) and antimycin A-sensitive succinate-cytochrome c oxidoreductase (complex III), were determined as described previously (Ortiz-Avila et al 2013), while cytochrome c oxidase (complex IV) activity was evaluated by the protocol described by Cortés-Rojo et al (2009).…”

Section: Determination Of the Activities Of The Etc Complexes And Mitmentioning

confidence: 99%

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Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats

Ortiz‐Avila

Gallegos‐Corona

Sánchez‐Briones

et al. 2015

J Bioenerg Biomembr

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Electron transport chain (ETC) dysfunction, excessive ROS generation and lipid peroxidation are hallmarks of mitochondrial injury in the diabetic liver, with these alterations also playing a role in the development of non-alcoholic fatty liver disease (NAFLD). Enhanced mitochondrial sensitivity to lipid peroxidation during diabetes has been also associated to augmented content of C22:6 in membrane phospholipids. Thus, we aimed to test whether avocado oil, a rich source of C18:1 and antioxidants, attenuates the deleterious effects of diabetes on oxidative status of liver mitochondria by decreasing unsaturation of acyl chains of membrane lipids and/or by improving ETC functionality and decreasing ROS generation. Streptozocin-induced diabetes elicited a noticeable increase in the content of C22:6, leading to augmented mitochondrial peroxidizability index and higher levels of lipid peroxidation. Mitochondrial respiration and complex I activity were impaired in diabetic rats with a concomitant increase in ROS generation using a complex I substrate. This was associated to a more oxidized state of glutathione, All these alterations were prevented by avocado oil except by the changes in mitochondrial fatty acid composition. Avocado oil did not prevented hyperglycemia and polyphagia although did normalized hyperlipidemia. Neither diabetes nor avocado oil induced steatosis. These results suggest that avocado oil improves mitochondrial ETC function by attenuating the deleterious effects of oxidative stress in the liver of diabetic rats independently of a hypoglycemic effect or by modifying the fatty acid composition of mitochondrial membranes. These findings might have also significant implications in the progression of NAFLD in experimental models of steatosis.

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Section: Discussionmentioning

confidence: 99%

Section: Determination Of the Activities Of The Etc Complexes And Mitmentioning

confidence: 99%

Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats

Ortiz‐Avila

Gallegos‐Corona

Sánchez‐Briones

et al. 2015

J Bioenerg Biomembr

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“…Similarly, studies have been carried out on different species of Aspergillus linking toxin production and the presence of oxidized lipids (Passi et al 1984;Reverberi et al 2010). Additionally, Cortés-Rojo et al (2009) found damage to the respiratory chain in S. cerevisiae with mitochondria sensitive to lipoperoxidation. It is important to mention that there are no reports describing the effects of stress and the presence of oxidized proteins and lipids in entomopathogenic fungi, and their consequences for conidial formation and germination.…”

Section: Discussionmentioning

confidence: 99%

Physiological and antioxidant response by Beauveria bassiana Bals (Vuill.) to different oxygen concentrations

Garza-López

Königsberg

Gómez-Quiroz

et al. 2011

World J Microbiol Biotechnol

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The effect of three levels of oxygen (normal atmosphere (21% O(2)), low oxygen (16% O(2)) and enriched oxygen (26% O(2))) on the production and germination of conidia by Beauveria bassiana was evaluated using rice as a substrate. The maximum yield of conidia was achieved under hypoxia (16% O(2)) after 8 days of culture (1.51 × 10(9) conidia per gram of initial dry substrate), representing an increase of 32% compared to the normal atmosphere. However, germination was reduced by at least 27% due to atmospheric modifications. Comparison of antioxidant enzyme activity (superoxide dismutases and catalases) with the oxidation profiles of biomolecules (proteins and lipids) showed that a decrease in catalase activity in the final days of culture coincided with an increase in the amount of oxidized lipids, showing that oxidative stress was a consequence of pulses of different concentrations of O(2). This is the first study describing oxidative stress induction by atmospheric modification, with practical implications for conidia production.

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“…Increased oxidative stress in the ITDϩRH group may result in more severe postischemic mitochondrial dysfunction. 39 It is plausible that this ultimately may be responsible for increased ischemic damage in the ITDϩRH group. We also observed increased calretinin levels in ITD rats exposed to RH.…”

Section: Discussionmentioning

confidence: 99%

Recurrent Hypoglycemia Exacerbates Cerebral Ischemic Damage in Streptozotocin-Induced Diabetic Rats

Dave

Tamariz

Desai

et al. 2011

Stroke

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Background and Purpose-Stroke and heart disease are the most serious complications of diabetes accounting for Ͼ65% of mortality among diabetics. Although intensive insulin therapy has significantly improved the prognosis of diabetes and its complications, it is associated with an elevated risk of recurrent hypoglycemia (RH). We tested the hypothesis that RH exacerbates cerebral ischemic damage in a rodent model of diabetes. Method-We determined the extent of neuronal death in CA1 hippocampus after global cerebral ischemia in control and streptozotocin-induced diabetic rats. Diabetic animals included an insulin-treated streptozotocin-diabetic (ITD) group and a group of ITD rats exposed also to 10 episodes of hypoglycemia (ITDϩrecurrent hypoglycemia: RH). Hypoglycemia (55 to 65 mg/dL blood glucose) was induced twice daily for 5 consecutive days. Results-As expected, uncontrolled diabetes (streptozotocin-diabetes, untreated animals) resulted in a 70% increase in ischemic damage as compared with the control group. Insulin treatment was able to lower ischemic damage by 64% as compared with the diabetic group. However, ITDϩRH rats had 44% more damage when compared with the ITD group. We also observed that free radical release from mitochondria is increased in ITDϩRH rats. Conclusions-This is the first report on the impact of RH in exacerbating cerebral ischemic damage in diabetic animals.Our results suggest that increased free radical release from mitochondria may be responsible for observed increased ischemic damage in ITDϩRH rats. RH thus may be an unexplored but important factor responsible for increased ischemic damage in diabetes. (Stroke. 2011;42:1404-1411.)Key Words: brain ischemia Ⅲ cardiac arrest Ⅲ diabetes Ⅲ free radicals Ⅲ glucose Ⅲ mitochondria Ⅲ stroke D iabetes is a devastating disease of epidemic proportions. It is estimated that 220 million patients are affected by diabetes worldwide. 1 Stroke and heart disease are the most serious complications of diabetes, because they account for approximately 65% of mortality among diabetics. 2 Epidemiological studies suggest that long-term diabetes increases the risk of cerebral ischemia as well as cardiovascular disease by 2 to 4 times as compared with the nondiabetic population. [3][4][5] The incidence of cerebral ischemia is greater in patients with Type 2 diabetes mellitus than Type 1 diabetes mellitus (T1DM). 3 Furthermore, cerebral infarction after ischemia is more extensive and common in diabetics, who also display slower recovery and worse survival rates than nondiabetic subjects. 6 Animal models corroborate these clinical observations and provide mechanistic insights into the pathophysiology of the effect of diabetes on cerebral ischemia. 7,8 It has been recognized that a high plasma glucose level is a key factor for the poor outcome observed after cerebral ischemia in diabetics. 9 Attaining tight glycemic control is a desirable goal for both patients with T1DM and Type 2 diabetes mellitus. Aggressive therapeutic interventions able to normalize glycohemog...

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Elucidation of the effects of lipoperoxidation on the mitochondrial electron transport chain using yeast mitochondria with manipulated fatty acid content

Cited by 37 publications

References 55 publications

Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats

Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats

Physiological and antioxidant response by Beauveria bassiana Bals (Vuill.) to different oxygen concentrations

Recurrent Hypoglycemia Exacerbates Cerebral Ischemic Damage in Streptozotocin-Induced Diabetic Rats

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