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Published on: September 16, 2020
Chlordecone (kepone) induces mitochondrial dysfunction in human cardiac tissue
Alexia Fundere1, Marie-Daniela Dubois2, Magalie Vatin Inamo1
1Cardiovascular Research Team (UR5_3 PC2E), University of the French West Indies (Université des Antilles), 97200 Fort de France, France; Department of Biology, Faculty of Natural and Exact Sciences, University of the French West Indies (Université des Antilles), 97110 Pointe-à-Pitre, France.
Chlordecone exposure impairs mitochondrial function in human heart cells, leading to uncoupling of oxidative phosphorylation. This mitochondrial dysfunction may cause abnormal cardiac cell responses, including oxidative stress.
Area of Science:
- Cardiology
- Toxicology
- Mitochondrial Biology
Background:
- Chlordecone exposure is linked to human health issues like prostate cancer and impaired fertility.
- Rodent studies suggest chlordecone inhibits magnesium-ATPase, but its mitochondrial toxicity in humans is poorly understood.
Purpose of the Study:
- To investigate the effects of chlordecone on mitochondrial function in human cardiac cells.
- To determine if chlordecone induces mitochondrial dysfunction in ex vivo human heart preparations.
Main Methods:
- Human atrial tissue was obtained from cardiac surgery patients.
- Cardiac preparations were exposed to chlordecone (5 nM and 50 nM) or vehicle for 24 hours.
- Mitochondrial function was assessed using high-resolution oxygraphy.
Main Results:
- Chlordecone exposure significantly impaired mitochondrial respiratory rates in human cardiac cells.
- Clinically relevant chlordecone concentrations increased state 2 respiration and maximal capacity, suggesting uncoupling.
- No change in state 3 respiration indicated disrupted mitochondrial oxidative phosphorylation.
Conclusions:
- Chlordecone at relevant concentrations induces mitochondrial dysfunction and uncoupling in human cardiac cells.
- This impairment may lead to adverse cardiac cell responses, such as aberrant calcium handling and oxidative stress.
- Further research is needed to understand the full implications of chlordecone-induced mitochondrial toxicity in the human heart.
