Respiratory chain complexes and membrane fatty acids composition in rat testis mitochondria throughout development and ageing

Vázquez-Memije, Martha Elisa; Cárdenas-Méndez, María J.; Tolosa, Adela; Hafidi, Mohammed El

doi:10.1016/j.exger.2005.03.006

Cited by 27 publications

(14 citation statements)

References 56 publications

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“…[21][22][23] Testis mitochondria presented lower values for Dcm and for repolarization potentials when compared with liver and kidney mitochondria (not shown, see Figures 1 and 2 liver mitochondria represented by the best values for RCR and ADP/O, which is in agreement with previous results. 21 It is also important to note that for testis mitochondria, we found a positive correlation between Dc and oxygen consumption (r ¼ 0.529, p ¼ 0.000).…”

Section: Tissue-specific Bioenergetic Parameterssupporting

confidence: 94%

“…This lower efficiency can be explained if we take into account that testis from adult animals present low levels of oxygen consumption, and ATP production depends highly on glucose metabolism in this tissue. 23 There are little available data relating proton leak with H 2 O 2 production for kidney 19 and liver 26 mitochondria and none concerning testis mitochondria. Superoxide (O 2 À ) and other ROS are formed as side-product of the respiratory chain within complex I and complex III.…”

Section: Discussionmentioning

confidence: 98%

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Proton leak modulation in testicular mitochondria affects reactive oxygen species production and lipid peroxidation

Rodrigues

Lacerda

Moreno

et al. 2010

Cell Biochemistry & Function

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Mitochondrial proton leak can account for almost 20% of oxygen consumption and it is generally accepted that this process contributes to basal metabolism. In order to clarify the role of basal proton leak in testicular mitochondria, we performed a comparative study with kidney and liver mitochondrial fractions. Proton leak stimulated by linoleic acid and inhibited by guanosine diphosphate (GDP) was detected, in a manner that was correlated with protein levels for uncoupling protein 2 (UCP2) in the three fractions. Modulation of proton leak had an effect on reactive oxygen species production as well as on lipid peroxidation, and this effect was also tissue-dependent. However, a possible role for the adenine nucleotide transporter (ANT) in testicular mitochondria proton leak could not be excluded. The modulation of proton leak appears as a possible and attractive target to control oxidative stress with implications for male gametogenesis.

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Section: Tissue-specific Bioenergetic Parameterssupporting

confidence: 94%

Section: Discussionmentioning

confidence: 98%

Proton leak modulation in testicular mitochondria affects reactive oxygen species production and lipid peroxidation

Rodrigues

Lacerda

Moreno

et al. 2010

Cell Biochemistry & Function

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“…The normal activities of mitochondrial respiratory complexes I and III and the increased activity of complex II suggest that SFR mitochondria have developed an adaptive mechanism to protect the mitochondrial respiratory complexes from oxidative stress. The mitochondrial respiratory complex activities have been shown to be highly susceptible to oxidative stress (56).…”

Section: Discussionmentioning

confidence: 99%

“…The activities of NADH-dehydrogenase (CI), succinate dehydrogenase (CII), succinate-cytochrome c oxidoreductase (CIII), and cytochrome c oxidase (CIV) were determined as described previously (56). Briefly, the activity of CI was measured by monitoring the oxidation of NADH in a solution containing 35 mM potassium phosphate buffer (pH 7.5), 0.2 mM NADH, and 1.7 mM potassium ferricyanide.…”

Section: Methodsmentioning

confidence: 99%

High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria

Ruiz-Ramírez

Chávez-Salgado

Peñeda-Flores

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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M. High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria. Am J Physiol Endocrinol Metab 301: E1198 -E1207, 2011. First published September 13, 2011 doi:10.1152/ajpendo.00631.2010.-Obesity, a risk factor for insulin resistance, contributes to the development of type 2 diabetes and cardiovascular diseases. The relationship between increased levels of free fatty acids in the liver mitochondria, mitochondrial function, and ROS generation in rat model of obesity induced by a high-sucrose diet was not sufficiently established. We determined how the bioenergetic functions and ROS generation of the mitochondria respond to a hyperlipidemic environment. Mitochondria from sucrose-fed rats generated H2O2 at a higher rate than the control mitochondria. Adding fatty acid-free bovine serum albumin to mitochondria from sucrose-fed rats significantly reduced the rate of H2O2 generation. In contrast, adding exogenous oleic or linoleic acid exacerbated the rate of H2O2 generation in both sucrose-fed and control mitochondria, and the mitochondria from sucrose-fed rats were more sensitive than the control mitochondria. The increased rate of H2O2 generation in sucrose-fed mitochondria corresponded to decreased levels of reduced GSH and vitamin E and increased levels of Cu/Zn-SOD in the intermembrane space. There was no difference between the levels of lipid peroxidation and protein carbonylation in the two types of mitochondria. In addition to the normal activity of Mn-SOD, GPX and catalase detected an increased activity of complex II, and upregulation of UCP2 was observed in mitochondria from sucrose-fed rats, all of which may accelerate respiration rates and reduce generation of ROS. In turn, these effects may protect the mitochondria of sucrose-fed rats from oxidative stress and preserve their function and integrity. However, in whole liver these adaptive mechanisms of the mitochondria were inefficient at counteracting redox imbalances and inhibiting oxidative stress outside of the mitochondria. reactive oxygen species; free fatty acid; metabolic syndrome; mitochondrial function; oxidative stress; uncoupling protein 2 ABDOMINAL OBESITY AND HIGH LEVELS of circulating free fatty acids (FFAs) have been indicated as primary contributors to acquired insulin resistance and hypertension because they induce oxidative stress that affects insulin signaling and nitric oxide availability (30, 11). Insulin resistance leads to continuous lipolysis within adipocytes, releasing FFAs into the local circulation, where they are transported into the liver. In the liver, FFAs can be incorporated into triglycerides that accumulate and lead to nonalcoholic fatty liver disease, the primary hepatic complication of obesity (13, 57). Oxidative stress and mitochondrial dysfunction have been shown to play a critical role in the initiation and progression of fatty liver to the more serious condition of nonalcoholic steatohepatitis in obesity models (15,21,38). Several studies using an animal model of fa...

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“…In this context, it was shown that aging increases the proportion of SFA in rat testis mitochondria, which was accompanied by a decreased activity of the mitochondrial respiratory enzymes [23]. Furthermore, we recently found that a 4-week palm oil-based HFD resulted in an increased saturation of skeletal muscle phospholipids [16].…”

Section: Introductionmentioning

confidence: 96%

High Fat Diet-Induced Changes in Mouse Muscle Mitochondrial Phospholipids Do Not Impair Mitochondrial Respiration Despite Insulin Resistance

et al. 2011

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BackgroundType 2 diabetes mellitus and muscle insulin resistance have been associated with reduced capacity of skeletal muscle mitochondria, possibly as a result of increased intake of dietary fat. Here, we examined the hypothesis that a prolonged high-fat diet consumption (HFD) increases the saturation of muscle mitochondrial membrane phospholipids causing impaired mitochondrial oxidative capacity and possibly insulin resistance.MethodologyC57BL/6J mice were fed an 8-week or 20-week low fat diet (10 kcal%; LFD) or HFD (45 kcal%). Skeletal muscle mitochondria were isolated and fatty acid (FA) composition of skeletal muscle mitochondrial phospholipids was analyzed by thin-layer chromatography followed by GC. High-resolution respirometry was used to assess oxidation of pyruvate and fatty acids by mitochondria. Insulin sensitivity was estimated by HOMA-IR.Principal FindingsAt 8 weeks, mono-unsaturated FA (16∶1n7, 18∶1n7 and 18∶1n9) were decreased (−4.0%, p<0.001), whereas saturated FA (16∶0) were increased (+3.2%, p<0.001) in phospholipids of HFD vs. LFD mitochondria. Interestingly, 20 weeks of HFD descreased mono-unsaturated FA while n-6 poly-unsaturated FA (18∶2n6, 20∶4n6, 22∶5n6) showed a pronounced increase (+4.0%, p<0.001). Despite increased saturation of muscle mitochondrial phospholipids after the 8-week HFD, mitochondrial oxidation of both pyruvate and fatty acids were similar between LFD and HFD mice. After 20 weeks of HFD, the increase in n-6 poly-unsaturated FA was accompanied by enhanced maximal capacity of the electron transport chain (+49%, p = 0.002) and a tendency for increased ADP-stimulated respiration, but only when fuelled by a lipid-derived substrate. Insulin sensitivity in HFD mice was reduced at both 8 and 20 weeks.Conclusions/InterpretationOur findings do not support the concept that prolonged HF feeding leads to increased saturation of skeletal muscle mitochondrial phospholipids resulting in a decrease in mitochondrial fat oxidative capacity and (muscle) insulin resistance.

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Respiratory chain complexes and membrane fatty acids composition in rat testis mitochondria throughout development and ageing

Cited by 27 publications

References 56 publications

Proton leak modulation in testicular mitochondria affects reactive oxygen species production and lipid peroxidation

Proton leak modulation in testicular mitochondria affects reactive oxygen species production and lipid peroxidation

High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria

High Fat Diet-Induced Changes in Mouse Muscle Mitochondrial Phospholipids Do Not Impair Mitochondrial Respiration Despite Insulin Resistance

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