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Cellular Targets of Photodynamic Therapy as a Guide to Mechanisms
Published in Barbara W. Henderson, Thomas J. Dougherty, Photodynamic Therapy, 2020
If mitochondrial oxidative phosphorylation is inhibited, one expects to see a reduction in cellular ATP levels. We observed this prediction occurring in a drug- and light-dose relation in tumor cells in vitro [15], and there was an apparent coordinate relationship between reduced cellular ATP levels and cell viability (assessed by trypan blue dye exclusion). By the propitious use of selected metabolic inhibitors—oligomycin and iodoacetate—we demonstrated that HPD photosensitization was additive to the iodoacetate-induced, but not to the oligomycin-induced, reduction in ATP levels. Since oligomycin inhibits the mitochondrial F0F1 ATP synthase, we deduced that mitochondria were very important targets of HPD photosensitization. Kessel [16] confirmed our findings of hematoporphyrin-induced photosensitization leading to reduction in cellular ATP levels.
Toxicological evaluation of the herbicide Palace® in Drosophila melanogaster
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Mayara B. Leão, Débora F. Gonçalves, Gabriela M. Miranda, Giovanna M. X. da Paixão, Cristiane L. Dalla Corte
The protocol used analyses five different states: (1) Proton-LEAK refers to the oxygen consumption resulting from the addition of pyruvate, proline, and malate independent of oxidative phosphorylation; (2) oxidative phosphorylation (OXPHOS) state is related to oxygen consumption in saturated ADP concentrations dependent on Complex I (CI), Complex II (CII) or Complex I + Complex II (CI&CII) after addition of its respective substrates; (3) LEAK is a non-phosphorylating resting state, representing oxygen consumption after enzymatic inhibition of the phosphorylation system by oligomycin; (4) electron transfer system (ETS) which is related to oxygen consumption in presence of the uncoupler FCCP; and (5) oxygen residual (ROX) which is respiration due to oxidative side reactions remaining after inhibition of the electron transfer-pathway by antimycin. In addition, the following ratios were calculated between respiratory states to measure mitochondrial functionality: coupling control ratio (L/P), leak control ratio (L/E), OXPHOS control ratio (P/E), excess capacity (E-P), Net OXPHOS control ratio ((P-L)/E), RCR – Respiratory control ratio (P/L).
Imidacloprid affects rat liver mitochondrial bioenergetics by inhibiting FoF1-ATP synthase activity
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Paulo F. V. Bizerra, Anilda R. J. S. Guimarães, Marcos A. Maioli, Fábio E. Mingatto
Subsequent experiments with carbonyl cyanide m-chlorophenylhydrazone (CCCP)-stimulated mitochondrial respiration were performed to examine the inhibitory influence of the compound on respiratory chain or ATP synthase. IMD did not markedly block CCCP-uncoupled respiration, indicating that only oxidative phosphorylation was inhibited (Figure 2). The same behavior was noted with oligomycin (FoF1-ATP synthase inhibitor) and carboxyatractyloside (ANT inhibitor).