Function mitochondrial

Ruthenium red inhibits the CICR activity at pM range. The site of ruthenium red action seems to be near or within ion channels. It also inhibits mitochondrial function. 

Henry, M.A., Nodes, E.E., Gao, D., Mazur, P., Critser. J.K. (1993). Cryopreservation of human spermatozoa. IV. The effects of cooling rate and warming rate on the maintenance of motility, plasma membrane integrity, and mitochondrial function. Fertil. and Steril. 60,911-918. 

Augustin, W. et al.. Beta-carotene cleavage products induce oxidative stress by impairing mitochondrial functions brain mitochondria are more sensitive than liver mitochondria, Free Rad. Biol. Med., 33, S326, 2002. 

PiaRigobello, M., Messori, L., Marcon, G., Cinellu, M.A., Bragadin, M., Folda, A., Scutari, G. and Bindoli, A. (2004) Gold complexes inhibit mitochondrial thioredoxin reductase consequences on mitochondrial functions. Journal of Inorganic Biochemistry, 98, 1634—1641. 

Recent studies by Crompton et al. have shown that oxidant stress may open a Ca-sensitive, non-selective pore in the inner mitochondrial membrane that is blocked by cyclosporin A (Crompton, 1990 Crompton and Costi, 1990). This pore opening results in massive mitochondrial swelling, dissipation of the transmembrane proton gradient and disruption of mitochondrial energy production (Crompton et al., 1992). Since mitochondria may play a role as a slow, high-capacity cytosolic calcium buffer (Isenberg et al., 1993), disruption of mitochondrial function may also contribute to calcium overload and cell injury. 

In recent studies on perfused rats hearts (Veitch et al., 1992), it was found that differences in the sensitivity of complexes 1-lV to ischaemic damage were dependent upon the duration of ischaemia and the presence of oxygen. The demonstration that complex 1 is a major defective site dependent upon isolation of mitochondria from homogenates of the tissue by in vitro methods seemed important to us. We therefore decided to attempt to make noninvasive measurements of mitochondrial function soon after reperfusion in transplanted rabbit kidneys by surface fluorescence (for mitochondrial NADH levels) and near infra-red spectroscopy (NIRS) for the redox state of cytaas. 

Coenzyme Q10 is an antioxidant essential for mitochondrial function. A dose of 1200 mg daily was associated with a slower decline in UPDRS scores than patients not receiving coenzyme Q10. Lower doses were no better than placebo, but the drug continues to be studied in doses up to 2400 mg daily. Many formulations contain vitamin E, and patients should not exceed recommended daily allowances of this vitamin, as bleeding times may be prolonged.42,43... 

Siems, W, Wiswedel, I, Salerno, C, Crifo, C, Augustin, W, Schild, L, Langhans, CD, and Sommerburg, O, 2005. Beta-carotene breakdown products may impair mitochondrial functions—Potential side effects of high-dose beta-carotene supplementation. J Nutr Biochem 16, 385-397. 

Despite a long-time studying of superoxide production by mitochondria, an important question is still debated does mitochondria produce superoxide under physiological conditions or superoxide release is always a characteristic of some pathophysiological disorders resulting in the damage of normal mitochondrial functions Uncertainties in this question arise due to the different results obtained with the use of respiratory inhibitors and different analytical methods. 

Brown, J. M. and Yamamoto, B. K. Effects of amphetamines on mitochondrial function role of free radicals and oxidative stress. Pharmacol. Ther. 99 45-53,2003. 

Aleo, M.D., Wyatt, R.D. and Schnellmann, R.G. (1991). The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. Toxicol. Appl. Pharmacol. 109 455 463. 

Oishi S. 1990. Effects of phthalic acid esters on testicular mitochondrial functions in the rat. Arch Toxicol 64 143-147. 

Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. The remaining genes provide instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of... 

Mitochondrial function. NO is able to react with transition metals such as iron, including those contained within haem groups. Even at low NO concentrations there is competition between oxygen and NO for reversible binding to cytochrome c oxidase. If mitochondrial 02 is low respiration slows, which may confer anti-apoptotic benefit to the cell. As NO concentration rises and peroxynitrite is formed, electron transport is irreversibly inhibited, there is increased production of superoxide and other reactive oxygen species and apoptosis occurs. 

Bromoethylamine (11.133, R = Br, Fig. 11.18) is a potent nephrotoxin used to create an experimental model of nephropathy. Its mechanism of toxicity is postulated to involve perturbation of mitochondrial function, and its metabolism was investigated in a search for toxic metabolites. In rat plasma, 2-bromoethylamine was converted to aziridine (11.134), formed by intramolecular nucleophilic substitution and bromide elimination [155], Another major metabolite was oxazolidin-2-one (11.136). This peculiar metabolite resulted from the reaction of 2-bromoethylamine with endogenous carbonate to form carbamic acid 11.135, followed by cyclization-elimination to oxazoli-din-2-one. In aqueous media containing excess carbonate, the formation of... 

Pepe, S., 2000, Mitochondrial function in ischemeia and reperfusion of the ageing heart. Clin. Exp. Pharmacol. Physiol., 27 745-750... 

Acetylation also plays a role in mitochondrial function and basal levels of ATP. Mouse studies have shown that in mice lacking a deacetylase (Sirt3), basal ATP levels were lower than that in normal mice. In organs such as the heart, kidneys, and liver, the ATP levels were decreased more than 50%. In concurrence with lower ATP levels, higher acetylation levels of mitochondrial proteins were also noted. When Sirt3 was added, ATP levels returned to normal. This work leads to the conclusion that acetylation controls the levels of ATP in the cell. 

Brain, muscle, and kidney cells, for example, all possess a few hundred or a few thousand mitochondria per cell. The human egg cell is remarkable in that it contains about 100,000 mitochondria. A sperm cell, in contrast, contains fewer than 100. New mitochondria are made as cells divide. The synthesis of new mitochondria requires that the proteins coded for by the nuclear genome and those coded for by the mitochondrial genome be mutually compatible to ensure optimal mitochondrial function. Since we can experience mutations in both nuclear and mitochondrial DNA, leading to alterations in mitochondrial proteins, long-term compatibility... 

Two mechanisms for loss of mitochondrial function have been suggested (i) damage caused by the chronic production of free radicals within the mitochondria and (ii) somatic mutations in the mitochondrial genome, which progressively accumulate during a lifetime. 

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