Oxygen consumption rate to evaluate mitochondrial dysfunction and toxicity in cardiomyocytes

Ahn, Dohee; Go, Ryeo‐Eun; Choi, Kyung‐Chul

doi:10.1007/s43188-023-00183-3

Cited by 3 publications

(2 citation statements)

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“…In cardiomyocytes, mitochondrial dysfunction is closely related to the development of heart diseases such as cardiac hypertrophy, heart failure, and ischemia–reperfusion injury 3,31,32 . Mitochondrial function can be detected by measuring mitochondrial OCR 33 . In the current study, the components of the OCR, such as basal respiration, proton leak, and ATP were decreased by Flu.…”

Section: Discussionsupporting

confidence: 46%

“…3,31,32 Mitochondrial function can be detected by measuring mitochondrial OCR. 33 In the current study, the components of the OCR, such as basal respiration, proton leak, and ATP were decreased by Flu. These results indicate that Flu decreases mitochondrial OCR, which, in turn, suggests that Flu influences oxidative phosphorylation in the mitochondria in cardiomyocytes.…”

Section: Discussionsupporting

confidence: 46%

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Fludioxonil induces cardiotoxicity via mitochondrial dysfunction and oxidative stress in two cardiomyocyte models

Seong,

Go,

Lee

et al. 2024

Environmental Toxicology

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Fludioxonil (Flu) is a phenylpyrrole fungicide and is currently used in over 900 agricultural products globally. Flu possesses endocrine‐disrupting chemical‐like properties and has been shown to mediate various physiological and pathological changes, such as apoptosis and differentiation, in diverse cell lines. However, the effects of Flu on cardiomyocytes have not been studied so far. The present study investigated the effects of Flu on mitochondria in AC16 human cardiomyocytes and H9c2 rat cardiomyoblasts. Flu decreased cell viability in a water‐soluble tetrazolium assay and mediated morphological changes suggestive of apoptosis in AC16 and H9c2 cells. We confirmed that annexin V positive cells were increased by Flu through annexin V/propidium iodide staining. This suggests that the decrease in cell viability due to Flu may be associated with increased apoptotic changes. Flu consistently increased the expression of pro‐apoptotic markers such as Bcl‐2‐associated X protein (Bax) and cleaved‐caspase 3. Further, Flu reduced the oxygen consumption rate (OCR) in AC16 and H9c2 cells, which is associated with decreased mitochondrial membrane potential (MMP) as observed through JC‐1 staining. In addition, Flu augmented the production of mitochondrial reactive oxygen species, which can trigger oxidative stress in cardiomyocytes. Taken together, these results indicate that Flu induces mitochondrial dysregulation in cardiomyocytes via the downregulation of the OCR and MMP and upregulation of the oxidative stress, consequently resulting in the apoptosis of cardiomyocytes. This study provides evidence of the risk of Flu toxicity on cardiomyocytes leading to the development of cardiovascular diseases and suggests that the use of Flu in agriculture should be done with caution and awareness of the probable health consequences of exposure to Flu.

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Section: Discussionsupporting

confidence: 46%