Radiocontrast Agent Diatrizoic Acid Induces Mitophagy and Oxidative Stress via Calcium Dysregulation

Ward, Dakota; Brown, Kathleen C.; Valentovic, Monica

doi:10.3390/ijms20174074

Cited by 10 publications

(9 citation statements)

References 85 publications

(96 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As a result, it is hypothesized that mitochondrial cells, as one of the first structures in cells, are damaged. In clinically relevant CM exposure, the previously suggested mechanism of misfolded or unfolded protein accumulation with subsequent endoplasmic reticulum stress does not play a critical role in decreasing cell viability ( 29 ). One of the main mechanisms of cellular death is a calcium overload within mitochondria.…”

Section: Pathogenesismentioning

confidence: 97%

“…This may be, in part, due to the concentrations of CM used in animal studies (usually over 5–100 times the concentrations found in plasma of patient undergoing CM administration). As proposed by Ward et al ( 29 ) changes of cellular homeostasis and cellular disarray induced in animal studies would not occur at clinical practice. The chemical structure of CM may suggest that free iodine particles lead to cytotoxicity.…”

Section: Pathogenesismentioning

confidence: 98%

“… Incidence of Cl-AKI reported in selected recent studies. Tsai et al ( 21 ); McDonald et al ( 23 ); Wilhelm-Leen et al ( 24 ); Schönenberger et al ( 27 ); Ward et al ( 29 ); Kiss and Hamar ( 30 ). CI-AKI, contrast induced acute kidney injury; PTCA, percutaneous transluminal coronary angioplasty; CTA, computed tomography angiography; CTP, computed tomography perfusion; NCCT, noncontrast computed tomography; CTCM, compute tomography with contrast; CATH, coronary vessels catheterisation; AKI-C, acute kidney injury control; CA-AKI-V, venous contrast application as the causative factor of CA-AKI, CA-AKI-A, arteria contrast application as the causative factor of CA-AKI.…”

Section: Incidencementioning

confidence: 99%

See 2 more Smart Citations

Contrast-induced acute kidney injury and its contemporary prevention

Sůva¹,

Kala²,

Poloczek³

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

The complexity and application range of interventional and diagnostic procedures using contrast media (CM) have recently increased. This allows more patients to undergo procedures that involve CM administration. However, the intrinsic CM toxicity leads to the risk of contrast-induced acute kidney injury (CI-AKI). At present, effective therapy of CI-AKI is rather limited. Effective prevention of CI-AKI therefore becomes crucially important. This review presents an in-depth discussion of CI-AKI incidence, pathogenesis, risk prediction, current preventive strategies, and novel treatment possibilities. The review also discusses the difference between CI-AKI incidence following intraarterial and intravenous CM administration. Factors contributing to the development of CI-AKI are considered in conjunction with the mechanism of acute kidney damage. The need for ultimate risk estimation and the prediction of CI-AKI is stressed. Possibilities of CI-AKI prevention is evaluated within the spectrum of existing preventive measures aimed at reducing kidney injury. In particular, the review discusses intravenous hydration regimes and pre-treatment with statins and N-acetylcysteine. The review further focuses on emerging alternative imaging technologies, alternative intravascular diagnostic and interventional procedures, and new methods for intravenous hydration guidance; it discusses the applicability of those techniques in complex procedures and their feasibility in current practise. We put emphasis on contemporary interventional cardiology imaging methods, with a brief discussion of CI-AKI in non-vascular and non-cardiologic imaging and interventional studies.

show abstract

Section: Pathogenesismentioning

confidence: 97%

Section: Pathogenesismentioning

confidence: 98%

Section: Incidencementioning

confidence: 99%

See 1 more Smart Citation

Contrast-induced acute kidney injury and its contemporary prevention

Sůva¹,

Kala²,

Poloczek³

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…The natural anti-oxidant tetramethylpyrazine suppressed ROS production, mitophagy, mitochondrial fragmentation, and renal tubular cell apoptosis in CI-induced AKI [126]. In addition, Mitophagy was also noticed in renal tubules in FA-induced AKI in rats [127], and in diatrizoic acid (DA)-induced renal tubular cell injury [128], but the precise role and regulation of mitophagy in these settings remain unknown.…”

Section: Mitophagy In Other Types Of Akimentioning

confidence: 99%

Mitophagy in Acute Kidney Injury and Kidney Repair

Wang

Cai

Tang

et al. 2020

Cells

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of renal tubules after severe or episodic AKI leads to renal fibrosis and, eventually, CKD. Recent studies highlight a key role of mitochondrial pathology in AKI development and abnormal kidney repair after AKI. As such, timely elimination of damaged mitochondria in renal tubular cells represents an important quality control mechanism for cell homeostasis and survival during kidney injury and repair. Mitophagy is a selective form of autophagy that selectively removes redundant or damaged mitochondria. Here, we summarize our recent understanding on the molecular mechanisms of mitophagy, discuss the role of mitophagy in AKI development and kidney repair after AKI, and present future research directions and therapeutic potential.

show abstract

“…Metabolic profiling of cultured kidney cells treated with different doses of cyclosporine A revealed a stark induction of glutathione metabolism, as well as alterations in amino acids and tricarboxylic acid cycle (TCA-cycle) intermediates [ 22 ]. Hence, the radiocontrast agent diatrizoic acid was also shown to induce an oxidative stress response [ 23 ]. Administration of the antiviral drug acyclovir, commonly causing acute kidney injury to rats, revealed excessive excretion of nitrogen containing metabolites to the urine [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Metabolic and Lipidomic Assessment of Kidney Cells Exposed to Nephrotoxic Vancomycin Dosages

Lagies

Pichler

Vladimirov

et al. 2021

IJMS

View full text Add to dashboard Cite

Vancomycin is a glycopeptide antibiotic used against multi-drug resistant gram-positive bacteria such as Staphylococcus aureus (MRSA). Although invaluable against resistant bacteria, vancomycin harbors adverse drug reactions including cytopenia, ototoxicity, as well as nephrotoxicity. Since nephrotoxicity is a rarely occurring side effect, its mechanism is incompletely understood. Only recently, the actual clinically relevant concentration the in kidneys of patients receiving vancomycin was investigated and were found to exceed plasma concentrations by far. We applied these clinically relevant vancomycin concentrations to murine and canine renal epithelial cell lines and assessed metabolic and lipidomic alterations by untargeted and targeted gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry analyses. Despite marked differences in the lipidome, both cell lines increased anabolic glucose reactions, resulting in higher sorbitol and lactate levels. To the best of our knowledge, this is the first endometabolic profiling of kidney cells exposed to clinically relevant vancomycin concentrations. The presented study will provide a valuable dataset to nephrotoxicity researchers and might add to unveiling the nephrotoxic mechanism of vancomycin.

show abstract

Radiocontrast Agent Diatrizoic Acid Induces Mitophagy and Oxidative Stress via Calcium Dysregulation

Cited by 10 publications

References 85 publications

Contrast-induced acute kidney injury and its contemporary prevention

Contrast-induced acute kidney injury and its contemporary prevention

Mitophagy in Acute Kidney Injury and Kidney Repair

Metabolic and Lipidomic Assessment of Kidney Cells Exposed to Nephrotoxic Vancomycin Dosages

Contact Info

Product

Resources

About