Restriction of glucose and fructose causes mild oxidative stress independently of mitochondrial activity and reactive oxygen species in Drosophila melanogaster.
Our recent study showed different effects of glucose and fructose overconsumption on the development of obese phenotypes in Drosophila. Glucose induced glucose toxicity due to the increase in circulating glucose, whereas fructose was more prone to induce obesity promoting accumulation of reserve lipids and carbohydrates (Rovenko et al., Comp. Biochem. Physiol. A Mol. Integr. Physiol. 2015, 180, 75-85). Searching for mechanisms responsible for these phenotypes in this study, we analyzed mitochondrial activity, mitochondrial density, mtROS production, oxidative stress markers and antioxidant defense in fruit flies fed 0.25%, 4% and 10% glucose or fructose. It is shown that there is a complex interaction between dietary monosaccharide concentrations, mitochondrial activity and oxidative modifications to proteins and lipids. Glucose at high concentration (10%) reduced mitochondrial protein density and consequently respiration in flies, while fructose did not affect these parameters. The production of ROS by mitochondria did not reflect activities of mitochondrial complexes. Moreover, there was no clear connection between mtROS production and antioxidant defense or between antioxidant defense and developmental survival, shown in our previous study (Rovenko et al., Comp. Biochem. Physiol. A Mol. Integr. Physiol. 2015, 180, 75-85). Instead, mtROS and antioxidant machinery cooperated to maintain a redox state that determined survival rates, and paradoxically, pro-oxidant conditions facilitated larva survival independently of the type of carbohydrate. It seems that in this complex system glucose controls the amount of oxidative modification regulating mitochondrial activity, while fructose regulates steady-state mRNA levels of antioxidant enzymes.
Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian National University, Ivano-Frankivsk 76018, Ukraine.
Bohdana M
BM
Rovenko
Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian National University, Ivano-Frankivsk 76018, Ukraine.
Olga I
OI
Kubrak
Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian National University, Ivano-Frankivsk 76018, Ukraine.
Dmytro V
DV
Gospodaryov
Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian National University, Ivano-Frankivsk 76018, Ukraine.
Ihor S
IS
Yurkevych
Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle-Upon-Tyne NE4 5PL, UK; Newcastle University Institute for Ageing, Newcastle University, Newcastle-Upon-Tyne NE4 5PL, UK.
Alberto
A
Sanz
Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian National University, Ivano-Frankivsk 76018, Ukraine. Electronic address: olehl@pu.if.ua.
Oleh V
OV
Lushchak
Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian National University, Ivano-Frankivsk 76018, Ukraine. Electronic address: lushchak@pu.if.ua.
Volodymyr I
VI
Lushchak
D000818:Animals; D004331:Drosophila melanogaster / Q000378:metabolism*; D005260:Female; D005632:Fructose / Q000008:administration & dosage*; D005947:Glucose / Q000008:administration & dosage*; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*
D017382:Reactive Oxygen Species; D005632:Fructose; D005947:Glucose
Antioxidant defense; Fructose; Glucose; Mitochondria; Oxidative stress; Reactive oxygen species (ROS)