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Methylglyoxal disrupts the functionality of rat liver mitochondria
Alessandro de Souza Prestes1, Matheus Mülling Dos Santos1, Jean Paul Kamdem2
1Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.
Abstract:
Methylglyoxal (MG) is a reactive metabolite derived from different physiological pathways. Its production can be harmful to cells via glycation reactions of lipids, DNA, and proteins. But, the effects of MG on mitochondrial functioning and bioenergetic responses are still elusive. Then, the effects of MG on key parameters of mitochondrial functionality were examined here. Isolated rat liver mitochondria were exposed to 0.1-10 mM of MG to determine its toxicity in the mitochondrial viability, membrane potential (Δψm), swelling and the superoxide (O2•-) production. Besides, mitochondrial oxidative phosphorylation parameters were analyzed by high-resolution respiratory (HRR) assay. In this set of experiments, routine state, PM state (pyruvate/malate), oxidative phosphorylation (OXPHOS), LEAK respiration, electron transport system (ETS) and oxygen residual (ROX) states were evaluated. HRR showed that PM state, OXPHOS CI-Linked, LEAK respiration, ETS CI/CII-Linked and ETS CII-Linked/ROX were significantly inhibited by MG exposure. MG also inhibited the complex II activity, and decreased Δψm and the viability of mitochondria. Taken together, our data indicates that MG is an inductor of mitochondrial dysfunctions and impairs important steps of respiratory chain, effects that can alter bioenergetics responses.
Insights
Methylglyoxal (MG) harms cells by damaging proteins and DNA. This study shows MG impairs mitochondrial function, inhibiting key respiratory chain steps and altering cellular energy production.
Area of Science:
- Biochemistry
- Cell Biology
- Mitochondrial Physiology
Background:
- Methylglyoxal (MG) is a reactive metabolite implicated in cellular damage through glycation.
- The specific impact of MG on mitochondrial function and bioenergetics remains largely unknown.
- Understanding MG's effects on mitochondria is crucial for comprehending its role in cellular pathology.
Purpose of the Study:
- To investigate the effects of methylglyoxal (MG) on isolated rat liver mitochondria.
- To assess MG's impact on mitochondrial viability, membrane potential, swelling, and superoxide production.
- To analyze the consequences of MG exposure on mitochondrial oxidative phosphorylation and respiratory chain activity.
Main Methods:
- Isolated rat liver mitochondria were treated with varying concentrations of methylglyoxal (0.1–10 mM).
- Mitochondrial viability, membrane potential (Δψm), swelling, and superoxide (O2•−) production were measured.
- High-resolution respirometry (HRR) was employed to evaluate mitochondrial respiration states, including oxidative phosphorylation (OXPHOS) and electron transport system (ETS) activities.
Main Results:
- Methylglyoxal significantly inhibited mitochondrial viability, decreased membrane potential (Δψm), and reduced superoxide production.
- High-resolution respirometry revealed that MG inhibited pyruvate/malate (PM) state, OXPHOS, LEAK respiration, and electron transport system (ETS) activities.
- Specifically, MG impaired Complex II activity, further contributing to mitochondrial dysfunction.
Conclusions:
- Methylglyoxal acts as an inducer of mitochondrial dysfunction.
- MG disrupts critical steps in the mitochondrial respiratory chain, leading to impaired bioenergetic responses.
- These findings highlight the detrimental role of MG in cellular energy metabolism and suggest its contribution to various pathologies.
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