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The parallel testing of isolated rat liver and kidney mitochondria reveals a calcium-dependent sensitivity to diclofenac and ibuprofen.

In: Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants. 2018. 217-228 ( ; 1-2)
DOI
as soon as is submitted to ZB.
A tissue-specific mode of mitochondrial impairments may appear as unintended side effect of diverse pharmaceuticals. The parallel isolation of mitochondria from rat liver and kidney tissues resulted in highly homogeneous mitochondrial populations as evidenced by electron microscopy. Mitochondrial testing demonstrated a relative robustness of liver and kidney mitochondria to ibuprofen and diclofenac, which reflects the fact that both nonsteroidal anti-inflammatory drugs (NSAIDs) typically present with a low risk of unintended side effects. The preincubation of liver and kidney mitochondria with 20μM calcium, a concentration that per se caused a late occurring mitochondrial permeability transition (MPT), induced a massively pronounced sensitivity to ibuprofen and diclofenac in a dose-dependent manner. As mitochondrial integrity and functionality are key issues for cellular homeostasis, toxicity on these organelles has to be assessed upon exposure to chemicals, toxins, and pharmaceutical interventions.
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Publication type Article: Edited volume or book chapter
Keywords Calcium-dependent Sensitivity ; Diclofenac ; Ibuprofen ; Kidney Mitochondria ; Mitochondrial Permeability Transition ; Parallel Testing ; Rat Liver
Reviewing status