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International Research Journal of Medicine and Medical Sciences
Vol. 1(4), October, 2013
Letter to the Editor

Necrosis and apoptosis in cancer therapy: Nutritional
facilitation and irreversible inactivation

GRN Jones

Cancer Research Unit, 30 Poplar Walk, London SE24 0BU, UK.
Dear Editor,
Necrosis (Trump et al., 1980) and apoptosis (Kerr et al., 1972; Muntané and De la Mata, 2010) are enzymically-mediated
modes of death theoretically available to the cancer cell in vivo. Haemorrhagic necrosis in a transplanted mouse sarcoma
(Gerber and Bernheim, 1938) is preceded by disruption of energy production, ATP leakage from mitochondria (Jones, 1979)
and a precipitous fall in the content of high-energy phosphate bonds (Jones, 1980a). Apoptosis depends on macromolecular
synthesis, and is blocked by pretreatment with cycloheximide (Wyllie et al., 1984). This communication considers situations in
which cell mortality in cancer treatments may be either facilitated by the provision of factors of dietary origin which are utilised
(Mosconi et al., 1989; Jones, 1992) in the process of destruction, or irreversibly blocked by mutagenic procedures.
Necrosis involves at least two enzymic steps. Initially phospholipid undergoes peroxidation. Secondly, hydrolysis by phospholipase A2 generates lysophosphatides and hydroperoxy fatty acids, which uncouple oxidative phosphorylation (Jones, 1992). The partial protection of interference with L-isoproterenol- and hydralazine-induced energy production by indomethacin (Jones, 1980b) in a transplanted mouse sarcoma indicates participation of a polyunsaturated fatty acid in the destructive process (Mosconi et al., 1989). Lower ratios of essential to saturated fatty acids have been reported in the plasma phospholipids of cancer patients; the greatest change was a 48% fall in the linoleic acid content of plasma cholesteryl esters (Mosconi et al., 1989). The total concentrations of w-6 and, particularly, of w-3 polyunsaturated fatty acids were very low in regions of intense cell proliferation in lung tissue from patients with lung cancer (Khyshiktuev et al., 2000). Apoptosis is more complex. The mandatory need for macromolecular synthesis (Wyllie et al., 1984) is thought to include the synthesis of nitric oxide synthase (Muntané and De la Mata, 2010) and antibodies. In paracetamol poisoning synthase is induced (Gardner et al., 1998; Hinson et al., 1998). Peroxynitrite derived from synthase activity reacts non-enzymically with tyrosine residues in proteins. Toxicity intensifies when alterations in antigenic profiles due to nitration provoke hostile responses from the immune system (Knight et al., 2001). Similar changes occur in the amyloid cascade during the terminal stages of Alzheimer's disease (Smith et al., 1997). Both endothelial and inducible nitric oxide synthase activities are elevated in cancer cells (Muntané and De la Mata, 2010). If tyrosine nitration of cancer cell proteins and the invocation of an immune response are central features of tumour apoptosis, a deficiency of the essential amino acid could compromise the therapeutic outcome. Under appropriate conditions phenothiazines (Jones, 1985) in low continuous dosage (Jones, 2010b) exert powerful anti- tumour activity; promethazine has shown success in the treatment of an anecdotal series of cancer cases (Jones, 2010a). Dietary supplementation with polyunsaturates is advised (Jones, 2010a, b). Although the initial injury inflicted on tumours by promethazine has been assumed to be necrosis, especially when the phenothiazine is initially given in conjunction with calcium (Jones, 2010b), in the later stages of treatment a limited role for apoptosis cannot be ruled out. Supplementation with tyrosine may be beneficial, as well as in therapies with hormone analogues in which necrosis appears not to feature. Both necrosis and apoptosis are vulnerable to mutagenic influences, and will be inactivated when genes coding for enzymes essential for the functioning of the mechanisms are deleted from the genome of a single malignant cell. In cancer patients the
establishment of cell clones (Jones, 2010a, b) in which both mechanisms are inactivated ensures a fatal outcome.
Keywords: Apoptosis, cancer, polyunsaturates, therapy, tyrosine.
Gardner CR, Heck DE, Yang CS, Thomas PE, Zhang XJ, DeGeorge GL, Laskin JD, Laskin DL, 1998. Role of nitric oxide in acetaminophen-induced
hepatotoxicity in the rat. Hepatology, 27:748-754. Hinson JA, Pike SL, Pumford NR, Mayeux PR, 1998. Nitrotyrosine-protein adducts in hepatic centrilobular areas fol owing toxic doses of acetaminophen in mice. Chem Jones GRN, 1979. Early mitochondrial damage in the induction of haemorrhagic necrosis in the Crocker sarcoma (S180) by endotoxin. J Cancer Res Clin Oncol, Jones GRN, 1980a. Early cutback in chemical energy production in the Crocker sarcoma (S180) undergoing haemorrhagic necrosis as a result of endotoxin administration. J Cancer Res Clin Oncol, 96:53-64. Jones GRN, 1980b. Prevention of drug-induced upset to energy production in the S180 sarcoma by inhibition of prostaglandin synthetase. Biochem Soc Trans, 8: 106- Jones GRN, 1985. Cancer therapy: phenothiazines in an unexpected role. Tumori, 71:563-569. Jones GRN, 1992. Cancer destruction in vivo through disrupted energy metabolism. Part II. Lipid peroxidation and cel death; drug resistance as a consequence of reversible cel ular injury. Physiol Chem Phys Med NMR, 24:181-194. Jones GRN, 2010a. A pilot study of the anti-neoplastic action of a phenothiazine in low dose. In: In the Darker Shadow of Science: the Subjugation of Cancer, iuniverse, Jones R, 2010b. Self-medication: the treatment of cancer with Phenergan [promethazine] with or without calcium. www.clearpublications.com/jones/phenergan- cancer/treatment.html (Accessed on 4 July, 2013). Kerr JFR, Wyl ie AH, Currie AR, 1972. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer, 26:239-57. Khyshiktuev BNS, Aganova IR, Zhilin IV, 2000. Fatty acid composition of lipids in lung tissue of patients with cancer. Vopr Onkol, 46(1):50-53. Knight TR, Kurtz A, Bajt ML, Hinson JA, Jaeschke H, 2001. Vascular and hepatocel ular peroxynitrite formation during acetaminophen toxicity: role of mitochondrial oxidative stress. Toxicol Sci, 62:212- 220. Mosconi C, Agradi E, Gambetta A, Bozzetti F, Gal i C, 1989. Decrease of polyunsaturated fatty acids and elevation of the oleic/stearic ratio in plasma and in red blood cel lipids of malnourished cancer patients. J Parenteral Enteral Nutr, 13:501-504. Muntané J, De la Mata M, 2010. Nitric oxide and cancer. World J Hepatology, 2:337-344. Smith MA, Richey HPL, Sayre LM, Beckman JS, Perry G, 1997. Widespread peroxy-nitrite mediated damage in Alzheimer's disease. J Neurosci, 17:2653-2657. Torreil es F, Salman-Tabchah S, Guérin MC, Torreil es J, 1999. Neurodegenerative disorders: the role of peroxynitrite. Brain Res Rev, 30:153-163. Trump BF, McDowel EM, Arstila AU, 1980. Cel ular reaction to injury. In: Principles of Pathobiology, 3rd Ed, RB Hil Jr, MF LaVia, (Eds.), Oxford University Press, New Wyl ie AH, Morris RG, Smith AL, 1984. Chromatin cleavage in apoptosis: association with condensed chromatin morphology and dependence on macromolecular

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