Trifloxystrobin-induced mitophagy through mitochondrial damage in human skin keratinocytes
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Published on: November 30, 2022
Yoonjeong Jang1, Ji-Eun Kim, Sang-Hee Jeong
1Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Korea.
Abstract:
Trifloxystrobin is a strobilurin class fungicide, the mode of action of which is to block the mitochondrial electron transport chain and inhibit energy production in fungi. Although adverse effects have been reported by occupational or environmental exposure of fungicides, the pathophysiological mechanism in human cells remains poorly understood. In the present study, we investigated the impact of trifloxystrobin on exposed skin at the cellular organelle level using HaCaT, the human skin keratinocyte cell line. Cells were treated with trifloxystrobin for 48 hr and trifloxystrobin showed detrimental effects on mitochondria evidenced by altered mitochondrial membrane potential and morphology. To identify autophagic degradation of the damaged mitochondria, confocal imaging and Western blotting were performed. Trifloxystrobin induced autophagy-related proteins in HaCaT cells. The mitochondrial reactive oxygen species scavenger mitoTEMPO was applied to further explore the mechanism of trifloxystrobin-mediated mitophagy in human skin cells. PINK1 and Parkin were overexpressed by trifloxystrobin, and mitoTEMPO alleviated the effects on mitophagy induction. Taken together, our findings indicated that mitochondrial damage and mitophagy may play a role in trifloxystrobin-induced toxicity in human keratinocytes and this could be suggested as a mechanism of cutaneous diseases developed by exposure.
Insights
Trifloxystrobin fungicide exposure damages mitochondria and triggers mitophagy in human skin cells. This cellular response may contribute to skin diseases from fungicide exposure.
Area of Science:
- Toxicology
- Cell Biology
- Dermatology
Background:
- Strobilurin fungicides like trifloxystrobin inhibit fungal energy production.
- The cellular mechanisms of fungicide toxicity in human skin are not well understood.
- Investigating trifloxystrobin's impact on human skin cells is crucial for understanding potential health risks.
Purpose of the Study:
- To investigate the cellular effects of trifloxystrobin on human skin keratinocytes (HaCaT cells).
- To elucidate the role of mitochondria and mitophagy in trifloxystrobin-induced toxicity.
- To explore the underlying mechanisms of potential skin damage from trifloxystrobin exposure.
Main Methods:
- HaCaT cells were treated with trifloxystrobin.
- Mitochondrial function (membrane potential, morphology) was assessed.
- Autophagy markers, mitophagy proteins (PINK1, Parkin), and reactive oxygen species were analyzed using confocal imaging and Western blotting.
- The effect of mitoTEMPO, a mitochondrial reactive oxygen species scavenger, was evaluated.
Main Results:
- Trifloxystrobin exposure altered mitochondrial membrane potential and morphology in HaCaT cells.
- Trifloxystrobin induced the expression of autophagy-related proteins and mitophagy markers (PINK1, Parkin).
- MitoTEMPO mitigated trifloxystrobin-induced mitophagy, suggesting a role for reactive oxygen species.
Conclusions:
- Trifloxystrobin causes mitochondrial damage and induces mitophagy in human keratinocytes.
- Mitochondrial dysfunction and mitophagy are implicated in trifloxystrobin toxicity.
- These findings suggest a potential mechanism for cutaneous diseases resulting from trifloxystrobin exposure.
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