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• W2969777510 endingPage "4074" @default.
• W2969777510 startingPage "4074" @default.
• W2969777510 abstract "Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital associated kidney damage. Potential mechanisms of CI-AKI may involve diminished renal hemodynamics, inflammatory responses, and direct cytotoxicity. The hypothesis for this study is that diatrizoic acid (DA) induces direct cytotoxicity to human proximal tubule (HK-2) cells via calcium dysregulation, mitochondrial dysfunction, and oxidative stress. HK-2 cells were exposed to 0-30 mg I/mL DA or vehicle for 2-24 h. Conversion of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and trypan blue exclusion indicated a decrease in mitochondrial and cell viability within 2 and 24 h, respectively. Mitochondrial dysfunction was apparent within 8 h post exposure to 15 mg I/mL DA as shown by Seahorse XF cell mito and Glycolysis Stress tests. Mitophagy was increased at 8 h by 15 mg I/mL DA as confirmed by elevated LC3BII/I expression ratio. HK-2 cells pretreated with calcium level modulators BAPTA-AM, EGTA, or 2-aminophenyl borinate abrogated DA-induced mitochondrial damage. DA increased oxidative stress biomarkers of protein carbonylation and 4-hydroxynonenol (4HNE) adduct formation. Caspase 3 and 12 activation was induced by DA compared to vehicle at 24 h. These studies indicate that clinically relevant concentrations of DA impair HK-2 cells by dysregulating calcium, inducing mitochondrial turnover and oxidative stress, and activating apoptosis." @default.
• W2969777510 created "2019-08-29" @default.
• W2969777510 creator A5018878943 @default.
• W2969777510 creator A5050660499 @default.
• W2969777510 creator A5056664665 @default.
• W2969777510 date "2019-08-21" @default.
• W2969777510 modified "2023-10-01" @default.
• W2969777510 title "Radiocontrast Agent Diatrizoic Acid Induces Mitophagy and Oxidative Stress via Calcium Dysregulation" @default.
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• W2969777510 doi "https://doi.org/10.3390/ijms20174074" @default.
• W2969777510 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6747199" @default.
• W2969777510 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31438500" @default.

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