Mitochondrial respiration

Bessman, S.P. Fonyo, A. (1966). The possible role of mitochondrial bound creatine kinase in regulation of mitochondrial respiration. Biochem. Biophys. Res. Commun. 22, 597-602. 

Dubey RK, Beg MU, Singh J. 1984. Effects of endosulfan and its metabolites on rat liver mitochondrial respiration and enzyme activities in vitro. Biochem Pharmacol 33 3405-3410. 

Nucleic acids are not the only biomolecules susceptible to damage by carotenoid degradation products. Degradation products of (3-carotene have been shown to induce damage to mitochondrial proteins and lipids (Siems et al., 2002), to inhibit mitochondrial respiration in isolated rat liver mitochondria, and to induce uncoupling of oxidative phosphorylation (Siems et al., 2005). Moreover, it has been demonstrated that the degradation products of (3-carotene, which include various aldehydes, are more potent inhibitors of Na-K ATPase than 4-hydroxynonenal, an aldehydic product of lipid peroxidaton (Siems et al., 2000). 

Siems, W, Sommerburg, O, Schild, L, Augustin, W, Langhans, CD, and Wiswedel, I, 2002. Beta-carotene cleavage products induce oxidative stress in vitro by impairing mitochondrial respiration. Faseb J 16,... 

B. Beltran, M. Quintero, E. Garcia-Zaragoza, E. O Connor, J.V. Esplugues, and S. Moncada, Inhibition of mitochondrial respiration by endogenous nitric oxide a critical step in Fas signaling. Proc. Natl. Acad. Sci. U.S.A. 99, 8892 (2002). 

The P/O ratio is the number of ATPs made for each O atom consumed by mitochondrial respiration. The P stands for high-energy phosphate equivalents, and the O actually stands for the number of I 02 s that are consumed by the electron transport chain. The full reduction of 02 to 2 H20 takes 4 electrons. Therefore, 2 electrons reduce of an 02. The oxidation of NADH to NAD and the oxidation of FADH2 to FAD are both 2-electron oxidations. O can be read as the transfer of 2 electrons. It s not quite as obscure as it sounds.2... 

As described earlier, superoxide is a well-proven participant in apoptosis, and its role is tightly connected with the release of cytochrome c. It has been proposed that a switch from the normal four-electron reduction of dioxygen through mitochondrial respiratory chain to the one-electron reduction of dioxygen to superoxide can be an initial event in apoptosis development. This proposal was supported by experimental data. Thus, Petrosillo et al. [104] have shown that mitochondrial-produced oxygen radicals induced the dissociation of cytochrome c from bovine heart submitochondrial particles supposedly via cardiolipin peroxidation. Similarly, it has been found [105] that superoxide elicited rapid cytochrome c release in permeabilized HepG2 cells. In contrast, it was also suggested [106] that it is the release of cytochrome c that inhibits mitochondrial respiration and stimulates superoxide production. 

LOX-dependent superoxide production was also registered under ex vivo conditions [55]. It has been shown that the intravenous administration of lipopolysaccharide to rats stimulated superoxide production by alveolar and peritoneal macrophages. O Donnell and Azzi [56] proposed that a relatively high rate of superoxide production by cultured human fibroblasts in the presence of NADH was relevant to 15-LOX-catalyzed oxidation of unsaturated acids and was independent of NADPH oxidase, prostaglandin H synthase, xanthine oxidase, and cytochrome P-450 activation or mitochondrial respiration. LOX might also be involved in the superoxide production by epidermal growth factor-stimulated pheochromo-cytoma cells [57]. 

The major types of adipose tissue are (1) white adipose tissue, which manufactures, stores, and releases lipid and (2) brown adipose tissue, which dissipates energy via uncoupled mitochondrial respiration. Obesity research includes evaluation of the activity of adrenergic receptors and their effect on adipose tissue with respect to energy storage and expenditure or thermogenesis. 

Mitochondrial respiration, insecticides and acaricides acting on, 14 348-349 Mitosis, in plants, 13 302 Mitotic entry inhibitors, 13 302-303 Mitotic sequence, disruption of,... 

Takahashi T. 1977. Biochemical studies on phthalic esters II. Effects of phthalic esters on mitochondrial respiration of rat liver. Biochem Pharmacol 26 19-24. 

A different and simpler approach to the measurement of P/O ratios came from the introduction of an oxygen electrode suitable for biochemical studies. Chance and Williams (1955) established conditions under which mitochondrial respiration, in the presence of excess substrate, was totally dependent on the amount of ADP available, i.e., the mitochondria were exhibiting respiratory control. From the change in potential when a known amount of ADP was admitted into the electrode vessel, the oxygen uptake and thus the P/O ratio could be determined, completely confirming the earlier results. 

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