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Intermittent fasting results in tissue-specific changes in bioenergetics and redox state.

Chausse B, Vieira-Lara MA, Sanchez AB, Medeiros MH, Kowaltowski AJ - PLoS ONE (2015)

Bottom Line: Although the consequences of CR are well studied, the effects of IF on redox status are not.No difference in mitochondrial bioenergetics or redox homeostasis was observed in skeletal muscles of IF animals.Overall, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain and protection against oxidative damage in the heart.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil.

ABSTRACT
Intermittent fasting (IF) is a dietary intervention often used as an alternative to caloric restriction (CR) and characterized by 24 hour cycles alternating ad libitum feeding and fasting. Although the consequences of CR are well studied, the effects of IF on redox status are not. Here, we address the effects of IF on redox state markers in different tissues in order to uncover how changes in feeding frequency alter redox balance in rats. IF rats displayed lower body mass due to decreased energy conversion efficiency. Livers in IF rats presented increased mitochondrial respiratory capacity and enhanced levels of protein carbonyls. Surprisingly, IF animals also presented an increase in oxidative damage in the brain that was not related to changes in mitochondrial bioenergetics. Conversely, IF promoted a substantial protection against oxidative damage in the heart. No difference in mitochondrial bioenergetics or redox homeostasis was observed in skeletal muscles of IF animals. Overall, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain and protection against oxidative damage in the heart.

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IF changes oxidative damage to biomolecules in a tissue-specific manner.(A) Carbonyl signals were quantified as described in Materials and Methods. (B) Malondaldehyde (MDA) levels were measured by HPLC as described in Materials and Methods. (C) Representative dot blots of NO2-tyr signals. (D) Average densitometric results for the dot blots presented in C. Data represent averages ± SEM and were compared using t tests (n = 4–5 animals). * p<0.05, ** p<0.01 vs AL.
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pone.0120413.g005: IF changes oxidative damage to biomolecules in a tissue-specific manner.(A) Carbonyl signals were quantified as described in Materials and Methods. (B) Malondaldehyde (MDA) levels were measured by HPLC as described in Materials and Methods. (C) Representative dot blots of NO2-tyr signals. (D) Average densitometric results for the dot blots presented in C. Data represent averages ± SEM and were compared using t tests (n = 4–5 animals). * p<0.05, ** p<0.01 vs AL.

Mentions: To determine the consequences of these tissue-specific modifications in antioxidant capacity, we measured the levels of protein carbonyls, MDA (a product of lipoperoxidation reactions) and nitro-tyrosine (NO2-Tyr) as markers for biomolecule oxidative damage (Fig. 5). In keeping with the finding that IF hearts were in a more reduced state, as indicated by their GSSG levels (Table 2), we found that protein carbonyls and MDA levels were reduced by IF in this tissue (Fig. 5A and 5B). On the other hand, the brain presented enhanced protein carbonylation under IF, which may be a reflection of lower catalase activity. In the liver, a small decrease in the NO2-Tyr signal and a robust increase in protein carbonylation levels was observed. The protein carbonylation effect may be a consequence of the slightly enchanced in oxidant generation in this tissue. There was no dietary-promoted difference in the measured oxidative damage markers in the skeletal muscle. Altogether, these data suggest that short-term IF affects redox balance in a tissue-specific manner, promoting protection against oxidative damage in the heart and leading to enhanced protein carbonylation in the brain and liver.


Intermittent fasting results in tissue-specific changes in bioenergetics and redox state.

Chausse B, Vieira-Lara MA, Sanchez AB, Medeiros MH, Kowaltowski AJ - PLoS ONE (2015)

IF changes oxidative damage to biomolecules in a tissue-specific manner.(A) Carbonyl signals were quantified as described in Materials and Methods. (B) Malondaldehyde (MDA) levels were measured by HPLC as described in Materials and Methods. (C) Representative dot blots of NO2-tyr signals. (D) Average densitometric results for the dot blots presented in C. Data represent averages ± SEM and were compared using t tests (n = 4–5 animals). * p<0.05, ** p<0.01 vs AL.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4352038&req=5

pone.0120413.g005: IF changes oxidative damage to biomolecules in a tissue-specific manner.(A) Carbonyl signals were quantified as described in Materials and Methods. (B) Malondaldehyde (MDA) levels were measured by HPLC as described in Materials and Methods. (C) Representative dot blots of NO2-tyr signals. (D) Average densitometric results for the dot blots presented in C. Data represent averages ± SEM and were compared using t tests (n = 4–5 animals). * p<0.05, ** p<0.01 vs AL.
Mentions: To determine the consequences of these tissue-specific modifications in antioxidant capacity, we measured the levels of protein carbonyls, MDA (a product of lipoperoxidation reactions) and nitro-tyrosine (NO2-Tyr) as markers for biomolecule oxidative damage (Fig. 5). In keeping with the finding that IF hearts were in a more reduced state, as indicated by their GSSG levels (Table 2), we found that protein carbonyls and MDA levels were reduced by IF in this tissue (Fig. 5A and 5B). On the other hand, the brain presented enhanced protein carbonylation under IF, which may be a reflection of lower catalase activity. In the liver, a small decrease in the NO2-Tyr signal and a robust increase in protein carbonylation levels was observed. The protein carbonylation effect may be a consequence of the slightly enchanced in oxidant generation in this tissue. There was no dietary-promoted difference in the measured oxidative damage markers in the skeletal muscle. Altogether, these data suggest that short-term IF affects redox balance in a tissue-specific manner, promoting protection against oxidative damage in the heart and leading to enhanced protein carbonylation in the brain and liver.

Bottom Line: Although the consequences of CR are well studied, the effects of IF on redox status are not.No difference in mitochondrial bioenergetics or redox homeostasis was observed in skeletal muscles of IF animals.Overall, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain and protection against oxidative damage in the heart.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil.

ABSTRACT
Intermittent fasting (IF) is a dietary intervention often used as an alternative to caloric restriction (CR) and characterized by 24 hour cycles alternating ad libitum feeding and fasting. Although the consequences of CR are well studied, the effects of IF on redox status are not. Here, we address the effects of IF on redox state markers in different tissues in order to uncover how changes in feeding frequency alter redox balance in rats. IF rats displayed lower body mass due to decreased energy conversion efficiency. Livers in IF rats presented increased mitochondrial respiratory capacity and enhanced levels of protein carbonyls. Surprisingly, IF animals also presented an increase in oxidative damage in the brain that was not related to changes in mitochondrial bioenergetics. Conversely, IF promoted a substantial protection against oxidative damage in the heart. No difference in mitochondrial bioenergetics or redox homeostasis was observed in skeletal muscles of IF animals. Overall, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain and protection against oxidative damage in the heart.

Show MeSH
Related in: MedlinePlus