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Copyright © Tarek Kakhia. All rights reserved. http://tarek.kakhia.org sulfur clusters and observed that oxygen uptake is abolished by H OCl and adenine nucleotides are lost. Also observed was, that irreversible oxidation of cyto chromes paralleled the loss of respiratory activity. One way of addressing the loss of oxygen uptake was by studying the effects of HOCl on succinate dependent electron transport.[37] Rosen et al.[31] found that levels of reductable cyto chromes in H Ocl - treated cells were normal, and these cells were unable to reduce them. Succinate dehydrogenase was also inhibited by H Ocl , stopping the flow of electrons to oxygen. Later studies revealed that Ubiquinol oxidase activity ceases first, and the still - active cyto chromes reduce the remaining quinone. The cytochromes then pass the electrons to oxygen, which explains why the cytochromes cannot be reoxidized, as observed by Rosen et al. However, this line of inquiry was ended when Albrich et al . found that cellular inactivation precedes loss of respiration by using a flow mixing system that allowed evaluation of viability on much smaller time scales. This group found that cells capable of respiring could not divide after exposure to H OCl. 5 . 2 . Depletion of adenine nucleotides Having eliminated loss of respiration Albrich et al . proposes that the cause of death may be due to metabolic dysfunction caused by depletion of adenine nucleotides. Barrette et al.[34] studied the loss of adenine nucleotides by studying the energy charge of H OCl - exposed cells and found that cells exposed to H OCl were unable to step up their energy charge after addition of nutrients. The conclusion was that exposed cells have lost the ability to regulate their adenylate pool, based on the fact that metabolite uptake was only 45 % deficient after exposure to HOCl and the observation that H OCl causes intracellular ATP hydrolysis. Also confirmed was that , at bacteriocidal levels of H OCl, cytosolic components are unaffected. So it was proposed that modification of some membrane - bound protein results in extensive ATP hydrolysis, and this, coupled with the cells inability to remove AMP from the cytosol, depresses metabolic function. One protein involved in loss of ability to regenerate ATP has been found to be ATP synthetase . Much of this research on respiration reconfirms the observation that relevant bacteriocidal reactions take place at the cell membrane . 39PDF Image | Chlorine Characteristics
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