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. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: Toxicology. 2019 Aug 30;427:152283. doi: 10.1016/j.tox.2019.152283

Figure 5. Proposed DCVC-induced mitochondrial dysfunction in HTR-8/SVneo cells.

Figure 5.

Overview and proposed partial sequence of DCVC-induced perturbations impacting mitochondrial structure and function. 1) At 6 h, mitochondrial basal OCR, reserve OCR and proton leak rate were elevated, while ATP coupling efficiency dropped significantly. 2) At 12 h, basal OCR declined significantly, accompanied by diminished maximum and reserve OCR, reduced ATP-linked OCR and decreased coupling efficiency, suggesting time-dependent progressive mitochondrial dysfunction. 3) Between 9 and 12 h, lipid peroxidation contributed to depolarization of mitochondrial membrane potential, however it did not contribute to other oxygen consumption-related mitochondrial perturbations, indicating lipid peroxidation may be a secondary effect of mitochondrial dysfunction.