Cell metabolism Glycolysis

As far as I can judge, all primitive cells had a basic reducing cell metabolism glycolysis, a citric acid cycle or its reverse, amino acid and base synthesis, while all maintained high K+, low Na+ and Cl-, moderate Mg2+, and very low Ca2+ (see Figure 2.3) by input and output pumps. Chemical... 

Cell metabolism induction. Methanol extract of STE, in collagen-producing cells, stimulated glycolysis by 80% in cartilage but was not affected in the other tissues. Medium alkaline phosphatase activity was unaffected. In the frontal bone and cartilage, [ H]hydroxyproline and [ H]proline contents were decreased. Neither was affected in the aorta. 

The process of glycolysis is without a doubt the single most ubiquitous pathway in all energy metabolism. Glycolysis can be characterized as a nearly universal process because it occurs in almost every living cell. It can occur in the ab-... 

ACTH has several other effects on adrenocortical cell metabolism. It increases the synthesis of adrenocortical cell phospholipids this may also have a long-term supportive role for increased steroidogenic capacity. It increases the rate of glycolysis in the adrenocortical cell this may have a supportive role in the supply of pyruvate for the mitochondrial steroid hydroxylases [32],... 

Barron ESG, Harrop GA. Studies on blood cell metabolism II. The effect of methylene blue and other dyes upon the glycolysis and lactic acid formation of mammalian and avian erythrocytes. J. Biol. Chem. 1928 79 65-87. 

The initial part of the glycolysis seqnence or pathway producing pyruvic acid or pyruvate is the same for both anaerobic and aerobic glycolysis. It would seem that this part should not be inhibited or otherwise interfered with, and only the anaerobic fermentation to yield lactic acid or lactate should be blocked, this being the main distinguishing featnre of cancer cell metabolism. 

Not resolved, however, is whether the inhibition of glycolysis per se can be an effective inhibitor of cancer cell metabolism, inasmuch as glycolysis is also involved in normal cell metabolism. 

However, as distinguished from the aerobic metabolism of normal cells, cancer cell metabolism is in the main anaerobic and does not invoke the carboxylic acid cycle, dependent on oxygen and fimdamental to cell respiration, as set forth in Chapter 3 for glycolysis. Thus, respiration of the cancerous cell is excluded from consideration. Hence, from this standpoint, the anticancer claims for amygdalin or laetrile can be viewed as missing the mark. That is, under this interpretation, cyanide would affect aerobic normal cells but not anaerobic cancerous cells. 

The Sigma catalog lists tyrosinase, the enzyme involved in melanoma. As mentioned elsewhere, among the inhibitors listed in the handbooks of enzyme inhibitors are ascorbic acid, or vitamin C, halide ion (the halides being chlorides, notably, but also fluorides, bromides, and iodides), butyric acid (a component of rancid butter), lactic acid (the final product of anaerobic glycolysis, as occurs in cancer cell metabolism, and a component also of sour milk and buttermilk), oxalic acid (e.g., as found in rhubarb and in wood sorrel), formic acid (a component of ant stings), even tyrosine itself, and toxic cyanide ion. And, as has been indicated, alpine sunflower/yueea extract may possibly serve as an enzyme inhibitor for tyrosinase. 

There are numerous th pies or treatments described in such books as Moss (1992) and Walters (1993). Some of these treatments (including those of folldoiic origin) utilize substances containing known enzyme inhibitors for one or anolh of the steps involved in glycolysis or cell metabolism. This may be snbstantiated by examining the two handbooks on enzyme inhibitors that have been pnblished, and have been repeatedly cited. 

Based on in vivo experimental results reported, vitamin C can also be viewed as an inhibitor for the key enzymes involved in carbohydrate metabolism or glycolysis, including lactate dehydrogenase, which is involved in cancer cell metabolism (Hoffman, 1999, p. 395). The inference is that vitamin C is an anticancer agent, as advanced by Pauling and Hoffer. 

In consequence, the inhibition of this particular enzyme has the potential of blocking cancer cell metabolism. The snbject was further discussed by the author in the articles, Enzyme Inhibitors for Cancer Cell Metabolism and Garlic and Allicin and Other Sulfur-Containing Componnds as Anticancer Agents, and in Hof nan (1999). There are still other metabolic pathways that can be considered, such as aminolysis, but in the main, cancer cells undergo anaerobic glycolysis. 

Krebs found that the pivotal mechanism of cell metabolism was a cycle. The cycle starts with glycolysis, which produces acetyl coenzyme A (acetyl CoA) fiom food molecules—carbohydrates, fats, and certain amino acids. The acetyl CoA reacts with oxaloacetate to form citric acid. The citric acid then goes through seven reactions that reconvert it back to oxaloacetate, and the cycle repeats. There is a net gain of twelve molecules of ATP per cycle. Not only does this cycle (known as the Krebs cycle, and also as the tri-carhoxyhc acid cycle and the citric acid cycle) generate the chemical energy to run the cell, it is also a central component of the syntheses of other biomolecules. 

The point at which the fungal cell can be considered dead is debatable [297]. It is not possible to reverse the lethal action of polyenes once sufflcient antibiotic molecules have combined with the cell membrane. Lethal levels of nystatin brought glycolysis of S. cerevisiae to a halt within 40 min [298] and 95% of the yeast cells were not viable after 30 min. Cell death inevitably follows destruction of membrane permeability. Whether the observed changes in cell metabolism, composition or morphology are causes or symptoms of death is unclear the sequence of antibiotic action in organisms other than fungi has received little attention. 

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