Age-related alterations in oxidatively damaged proteins of mouse skeletal muscle mitochondrial electron transport chain complexes

Choksi, Kashyap; Nuss, Jonathan E.; DeFord, James H.; Papaconstantinou, John

doi:10.1016/j.freeradbiomed.2008.06.006

Cited by 60 publications

(43 citation statements)

References 56 publications

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“…In particular, carbonylation of complex I subunits in the range of 20 to 75 kDa was detected, and the extent of inhibition of complex I activity seemed to be directly correlated with the extent of protein carbonylation (Taylor et al, 2003;Keeney et al, 2006;Choksi et al, 2008;Folbergrová et al, 2010). Carbonylation of several subunits of complex I, such as NDUFS1, NDUFS2, NDUFV1, NDUFA9, ND4, and NDUFS4, has been reported previously (Wen and Garg, 2004;Keeney et al, 2006;Choksi et al, 2008).…”

Section: Discussionsupporting

confidence: 59%

“…No difference in ROS production was observed when succinate was used as respiratory substrate (data not shown). Complex I is particularly susceptible to oxidative stress (Taylor et al, 2003;Choksi et al, 2004), and functional defects of the complex have been associated with nitrosylation and/or carbonylation of its subunits (Choksi et al, 2008;Folbergrová et al, 2010).…”

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confidence: 99%

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Rat Embryo Exposure to All-Trans Retinoic Acid Results in Postnatal Oxidative Damage of Respiratory Complex I in the Cerebellum

Signorile

Sardaro²,

Rasmo³

et al. 2011

Mol Pharmacol

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The results of the present work show that the exposure of pregnant rats to low doses of all-trans-retinoic acid (ATRA) (2.5 mg/kg body weight) results in postnatal dysfunction of complex I of the respiratory chain in the cerebellum of the offspring. ATRA had no effect on the postnatal expression of complex I and did not exert any direct inhibitory effect on the enzymatic activity of the complex. The ATRA embryonic exposure resulted, however, in a marked increase in the level of carbonylated proteins in the mitochondrial fraction of the cerebellum, in particular of complex I subunits. The postnatal increase of the carbonylated proteins correlated directly with the inhibition of the activity of complex I. ATRA had, on the other hand, no effect on oxygen free-radical scavengers. It is proposed that embryonic exposure to ATRA results in impairment of protein surveillance in the cerebellum, which persists after birth and results in accumulation of oxidatively damaged complex I.

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Section: Discussionsupporting

confidence: 59%

mentioning

confidence: 99%

Rat Embryo Exposure to All-Trans Retinoic Acid Results in Postnatal Oxidative Damage of Respiratory Complex I in the Cerebellum

Signorile

Sardaro²,

Rasmo³

et al. 2011

Mol Pharmacol

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“…OH : radicals are short-lived, and react close to where they are produced (Latch & McNeill, 2006). This implies that membrane proteins (respiratory enzymes, F 1 F 0 ATPase) and lipids are especially in danger of oxidation by this species, as also assumed by other authors (Choksi et al, 2008). One could argue that with an interrupted respiratory chain the electron flow and thereby also ROS stress would immediately be stopped.…”

Section: Ros-mediated Damage To Membrane Proteins Probably Causes Celmentioning

confidence: 79%

The respiratory chain is the cell's Achilles' heel during UVA inactivation in Escherichia coli

et al. 2010

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Solar disinfection (SODIS) is used as an effective and inexpensive tool to improve the microbiological quality of drinking water in developing countries where no other means are available. Solar UVA light is the agent that inactivates bacteria during the treatment. Damage to bacterial membranes plays a crucial role in the inactivation process. This study showed that even slightly irradiated cells (after less than 1 h of simulated sunlight) were strongly affected in their ability to maintain essential parts of their energy metabolism, in particular of the respiratory chain (activities of NADH oxidase, succinate oxidase and lactate oxidase were measured). The cells' potential to generate ATP was also strongly inhibited. Many essential enzymes of carbon metabolism (glucose-6-phosphate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase, lactate dehydrogenase and malate dehydrogenase) and defence against oxidative stress (catalases and glutathione-disulfide reductase) were reduced in their activity during SODIS. The work suggests that damage to membrane enzymes is a likely cause of membrane dysfunction (loss of membrane potential and increased membrane permeability) during UVA irradiation. In this study, the first targets on the way to cell death were found to be the respiratory chain and F 1 F 0 ATPase.

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“…We were not able to find data on C-I activity and pulmonary development. In murine heart, kidney, and muscle, the activity of C-I was reported to be the highest in young animals with a gradual reduction with the age (31)(32)(33). In humans, C-I activity in muscle mitochondria was greater in premature neonates compared with older infants and children (34).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Dysfunction Contributes to Alveolar Developmental Arrest in Hyperoxia-Exposed Mice

Ratner¹,

Starkov²,

Matsiukevich³

et al. 2009

Am J Respir Cell Mol Biol

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This study investigated whether mitochondrial dysfunction contributes to alveolar developmental arrest in a mouse model of bronchopulmonary dysplasia (BPD). To induce BPD, 3-day-old mice were exposed to 75% O 2 . Mice were studied at two time points of hyperoxia (72 h or 2 wk) and after 3 weeks of recovery in room air (RA). A separate cohort of mice was exposed to pyridaben, a complex-I (C-I) inhibitor, for 72 hours or 2 weeks. Alveolarization was quantified by radial alveolar count and mean linear intercept methods. Pulmonary mitochondrial function was defined by respiration rates, ATP-production rate, and C-I activity. At 72 hours, hyperoxic mice demonstrated significant inhibition of C-I activity, reduced respiration and ATP production rates, and significantly decreased radial alveolar count compared with controls. Exposure to pyridaben for 72 hours, as expected, caused significant inhibition of C-I and ADP-phosphorylating respiration. Similar to hyperoxic littermates, these pyridaben-exposed mice exhibited significantly delayed alveolarization compared with controls. At 2 weeks of exposure to hyperoxia or pyridaben, mitochondrial respiration was inhibited and associated with alveolar developmental arrest. However, after 3 weeks of recovery from hyperoxia or 2 weeks after 72 hours of exposure to pyridaben alveolarization significantly improved. In addition, there was marked normalization of C-I and mitochondrial respiration. The degree of hyperoxia-induced pulmonary simplification and recovery strongly (r 2 5 0.76) correlated with C-I activity in lung mitochondria. Thus, the arrest of alveolar development induced by either hyperoxia or direct inhibition of mitochondrial oxidative phosphorylation indicates that bioenergetic failure to maintain normal alveolar development is one of the fundamental mechanisms responsible for BPD.

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Age-related alterations in oxidatively damaged proteins of mouse skeletal muscle mitochondrial electron transport chain complexes

Cited by 60 publications

References 56 publications

Rat Embryo Exposure to All-Trans Retinoic Acid Results in Postnatal Oxidative Damage of Respiratory Complex I in the Cerebellum

Rat Embryo Exposure to All-Trans Retinoic Acid Results in Postnatal Oxidative Damage of Respiratory Complex I in the Cerebellum

The respiratory chain is the cell's Achilles' heel during UVA inactivation in Escherichia coli

Mitochondrial Dysfunction Contributes to Alveolar Developmental Arrest in Hyperoxia-Exposed Mice

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