Transport oxygen dependence supply

Acyl-CoA molecules are desaturated in ER membrane in the presence of NADH and 02. All components of the desaturase system are integral membrane proteins that are apparently randomly distributed on the cytoplasmic surface of the ER. The association of cytochrome b5 reductase (a flavoprotein), cytochrome b5, and oxygen-dependent desaturases constitutes an electron transport system. This system efficiently introduces double bonds into long-chain fatty acids (Figure 12.15). Both the flavoprotein and cytochrome b5 (found in a ratio of approximately 1 30) have hydrophobic peptides that anchor the proteins into the microsomal membrane. Animals typically have A9, A6, and A5 desaturases that use electrons supplied by NADH via the electron transport system to activate the oxygen needed to create the double bond. Plants contain additional desaturases for the A12 and A15 positions. 

The operation of the cycle requires a supply of the oxidizing agents NAD and FAD. The cycle is dependent on reactions of the electron transport chain to supply the necessary NAD and FAD (Section 13.6). Because oxygen is the final acceptor of electrons in the electron transport chain, the continued operation of the citric acid cycle depends ultimately on an adequate supply of oxygen. 

Most tissues are constantly dependent on a supply of molecular oxygen (O2) to maintain their oxidative metabolism. Due to its poor solubility, O2 is bound to hemoglobin for transport in the blood (see p. 280). This not only increases the oxygen transport capacity, but also allows regulation of O2 uptake in the lungs and O2 release into tissues. 

The cellular mechanism of direct cephalosporin-induced nephrotoxicity may include several possible actions of the cephalosporins. Nephrotoxic cephalosporins are known to induce lipid peroxidation and cellular membrane damage, acylate cellular proteins, and/or interfere with mitochondrial respiration. Mitochondrial respiration appears to be inhibited due to acylation of mitochondrial transporters for metabolic substrates, thereby depriving mitochondria of the necessary intermediates to utilize oxygen. Ultimately, the formation of adenosine triphosphate (ATP), needed to supply cellular energy, also declines to inhibit energy-dependent cellular functions. 

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