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Preparation of Mitochondrial Enriched Fractions for Metabolic Analysis in Drosophila
Published on: September 30, 2015
Mancozeb impairs mitochondrial and bioenergetic activity in Drosophila melanogaster
Miriane Acosta Saraiva1, Nelson Rodrigues de Carvalho1,2, Illana Kemmerich Martins1
1Oxidative Stress and Cell Signaling Research Group, Universidade Federal do Pampa, Campus São Gabriel, 97300-000, São Gabriel, RS, Brazil.
Abstract:
Mancozeb (MZ) is a broad-spectrum fungicide used worldwide in several crops. Neurological disorders in humans and animals have been associated with exposure to this compound by mechanisms still not fully understood. Drosophila melanogaster represents a reliable model in toxicological studies, presenting genetic and biochemical similarities with mammals. In this study, D. melanogaster flies were exposed for 15 days to MZ through the food (5 and 10 mg/mL). After that period, the efficiency of mitochondrial respiration complexes and metabolic markers were analyzed and evaluated. Flies presented weight loss, lower glucose, trehalose, and glycogen levels, and augmented levels of triglycerides concerning control (non-treated group). Acetyl-CoA Synthetase (ACeCS-1) and Acyl-Coenzyme Synthetase (ACSL1) contents were unchanged by MZ treatment. Mitochondrial respiration of flies was targeted by MZ treatment, evidenced by a decrease in oxygen consumption and bioenergetics rate and inhibition in mitochondrial complexes I/II. These results suppose that an impairment in mitochondrial respiration jointly with reduced levels of energetic substrates might be a mechanism involved in MZ deleterious effects, possibly by the limitation of ATP's availability, necessary for essential cellular processes.
Insights
Mancozeb fungicide exposure impairs mitochondrial respiration and reduces energy stores in fruit flies. This suggests a potential mechanism for its neurological effects, possibly by limiting cellular energy availability.
Area of Science:
- Toxicology
- Neuroscience
- Biochemistry
Background:
- Mancozeb (MZ) is a widely used fungicide with suspected neurological effects.
- The precise mechanisms underlying MZ's toxicity are not fully understood.
- Drosophila melanogaster serves as a valuable model for toxicological research due to its genetic and biochemical similarities to mammals.
Purpose of the Study:
- To investigate the toxicological effects of Mancozeb on mitochondrial function and metabolic markers in Drosophila melanogaster.
- To explore potential mechanisms of MZ-induced neurotoxicity using a fly model.
Main Methods:
- Drosophila melanogaster were exposed to Mancozeb (5 and 10 mg/mL) in their diet for 15 days.
- Analysis of metabolic markers including glucose, trehalose, glycogen, and triglycerides.
- Evaluation of mitochondrial respiration, oxygen consumption, and the activity of mitochondrial complexes I/II.
Main Results:
- Mancozeb exposure led to significant weight loss and altered metabolic profiles in flies.
- Reduced levels of glucose, trehalose, and glycogen were observed, alongside increased triglyceride levels.
- Mancozeb treatment inhibited mitochondrial complexes I/II, decreased oxygen consumption, and lowered the overall bioenergetic rate.
Conclusions:
- Impaired mitochondrial respiration and reduced energy substrates are likely mechanisms contributing to Mancozeb's deleterious effects.
- Mancozeb toxicity may result from a limitation in ATP availability, crucial for cellular functions.
- These findings highlight the potential neurotoxic impact of Mancozeb and underscore the utility of Drosophila as a model organism.
