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At least 343 records · Page 19Linked to original sources
PubMed1995

Effect of NDGA on beef heart mitochondria and EMT6 mouse mammary carcinoma cells.

The inhibition of mitochondrial succinate cytochrome c reductase by nordihydroguaiaretic acid (NDGA) was measured in vitro under aerobic and hypoxic conditions. The photodynamic effect of NDGA on EMT6 mouse mammary carcinoma cells was also investigated in vitro under aerobic and hypoxic conditions. NDGA strongly inhibited succinate cytochrome c reductase, which contains the mitochondrial electron transport Complexes II and III. By comparing the I50 values of aerobic and hypoxic assays, NDGA inhibition was found to be oxygen-independent. This finding suggests that oxygen is not involved in the inhibitory effect of mitochondrial respiration by NDGA. Similarly, our data demonstrate that NDGA-induced cytotoxicity towards EMT6 tumor cells is neither light-dependent nor oxygen-dependent. A dose-dependent loss of viability of EMT6 cell was observed although the toxicity of NDGA towards EMT6 cells was not strong, with an LC50 in the 200 microM range. NDGA caused a depletion of mitochondrial sulfhydryl groups. Sulfhydryl compounds, GSH and cysteine, prevented the inhibition of succinoxidase activity by NDGA. This suggests that NDGA exerts its biological effects by the depletion of sulfhydryl groups in key biochemical systems related to mitochondrial function.

Aerobiosis↗
PubMed1996

Differential inhibitory action of nitric oxide and peroxynitrite on mitochondrial electron transport.

Various authors have suggested that nitric oxide (.NO) exerts cytotoxic effects through the inhibition of cellular respiration. Indeed, in intact cells .NO inhibits glutamate-malate (complex I) as well as succinate (complex II)-supported mitochondrial electron transport, without affecting TMPD/ascorbate (complex IV)-dependent respiration. However, experiments in our lab using isolated rat heart mitochondria indicated that authentic .NO inhibited electron transport mostly by reversible binding to the terminal oxidase, cytochrome a3, having a less significant effect on complex II- and no effect on complex I-electron transport components. The inhibitory action of .NO was more profound at lower oxygen tensions and resulted in differential spectra similar to that observed in dithionite-treated mitochondria. On the other hand, continuous fluxes of .NO plus superoxide (O.(2)(-)), which lead to formation of micromolar steady-state levels of peroxynitrite anion (ONOO-), caused a strong inhibition of complex I- and complex II-dependent mitochondrial oxygen consumption and significantly inhibited the activities of succinate dehydrogenase and ATPase, without affecting complex IV-dependent respiration and cytochrome c oxidase activity. In conclusion, even though nitric oxide can directly cause a transient inhibition of electron transport, the inhibition pattern of mitochondrial respiration observed in the presence of peroxynitrite is the one that closely resembles that found secondary to .NO interactions with intact cells and strongly points to peroxynitrite as the ultimate reactive intermediate accounting for nitric oxide-dependent inactivation of electron transport components and ATPase in living cells and tissues.

Adenosine Triphosphatases↗
PubMed1996

Creation and characterization of mitochondrial DNA-depleted cell lines with "neuronal-like" properties.

Mitochondrial dysfunction and attendant bioenergetic defects are increasingly recognized as playing an important role in neurodegenerative disorders. The increased attention on mitochondrial involvement points to the need for developing cell lines that have neuron-like characteristics for the genetic analysis and modeling of these diseases. We describe the creation of respiratory-deficient SH-SY5Y neuroblastoma cell lines (rho zero 64/5) by selectively depleting mitochondrial DNA through prolonged exposure to ethidium bromide. Oxygen consumption in these cells and activities of the electron transport chain enzyme complexes I and IV that contain subunits encoded by the mitochondrial genome are eliminated. In contrast, the function of complex II, a nuclear-encoded electron transport chain component, is largely intact in these cells. The rho zero 64/5 cells retain the ability to differentiate into cells with neuron-like phenotypes following treatment with phorbol ester or retinoic acid. Normal respiratory function is recovered by repopulation of rho zero 64/5 cells with exogenous human platelet mitochondria. The rho zero 64/5 cell line serves as a valuable model for the study of neurologic diseases suspected of involving mitochondrial dysfunction.

Blood Platelets↗
PubMed1987

Rapid, quantitative microassay for the monokine respiration inhibitory factor.

The murine monokine respiration inhibitory factor (RIF) induces lesions at Complex I and Complex II of the mitochondrial electron transport chain (ETC) of tumor cells; these lesions in the ETC appear closely linked with cytostasis of the targets. In this report we describe the use of the sensitive murine mammary adenocarcinoma line EMT-6 in a colorimetric microassay for the effects of RIF on the ETC and target replication. The participation of cytolytic molecules in this assay system was excluded because of the resistance of the target to their effects. The endpoint for the assay was the ETC-mediated reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) to its colored formazan. The two major coupling sites of MTT in the ETC of EMT-6 cells are shown to be proximal to Coenzyme Q, detected either by malate oxidation through Complex I or succinate oxidation through Complex II. The assay was sensitive to both RIF-induced lesions at these dehydrogenases and to the cytostasis-linked reduction in target cell number. The assessment of ETC lesions by this microassay correlated directly with that determined by the less sensitive polarimetric assay based on oxygen consumption. We demonstrate the application of this microassay to parameters for the production of RIF by activated murine macrophages, and to initial molecular characterization of this mediator.

Animals↗