Mitochondria function

As it is similar to a fatty acid, it forms an acyl CoA and a carnitine derivative. This depletes CoA from the intramitochondrial pool and carnitine. Also, valproic acid is metabolized to an unsaturated fatty acid analogue, which is incorporated into p-oxidation in mitochondria. The reactive analogue depletes GSH and damages mitochondria. Function is compromised and ATP depleted. 

Approximate Size Function in Mitochondria Function in Apoptosis... 

Ott M, Robertson JD, Gogvadze V,Zhivotovsky B, Orrenius S (2002) Cytochrome c release from mitochondria proceeds by a two-step process. Proc Natl Acad Sci USA 99 1259-1263 Schroeter H, Boyd CS, Ahmed R, Spencer JPE, Duncan RF, Rice-Evans C, Cadenas E (2003) JNK-mediated modulation of brain mitochondria function new target proteins for JNK-signaling in mitochondria-dependent apoptosis. Biochem J 372 359-369 Alvarez S, Valdez LB,Zaobornyj T, Boveris A (2003) Oxygen dependence of mitochondrial nitric oxide synthase activity. Biochem Biophys Res Commun 305 771-775... 

ATP is uncoupled from electron transport. Other compounds affect mitochondrial function by inhibiting the electron transport chain at one or more specific sites, such as the toxic metabolite of MPTP which inhibits complex I (see Chapter 7). The toxic metabolite of hexachlorobutadiene is believed to be nephrotoxic due to inhibition of mitochondria function in the proximal tubular cells. 

In general it is assumed that WAT and BAT develop from different precursor cells. However, a common precursor for both cannot be ruled out and the possible transformation of BAT into WAT has been considered. The conversion from BAT to WAT would be correlated with a decrease in BAT-specific gene products such as UCP. Recently, experiments have suggested that under certain conditions WAT might take on a BAT-like phenotype, with increased mitochondria function. 

Results from five taxonomic kingdoms have been reported for TBT [71-74], The main toxic effects reported have been endocrine disruption [75] and mitochondria function impairment [76], Even so, the molecular mechanisms involving TBT inhibition are far from understood. Along with the sites mentioned above, biological membranes have been suggested as targets because of the high-lipophilicity of TBT [71,77]. 

JNK can also stabilize the proapoptotic p53 through phosphorylation [78] (Fig. 4). Once phosphorylated, p53 can impair mitochondria function and induce the permeability transition through its mediator p53-regulated apoptosis-inducing protein 1 (p53AIPl), a mitochondrial protein [79]. Furthermore, the expression of the proapoptotic Bax is regulated by p53 [80]. Alternatively,... 

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