FIG. 53 FORMATION AND DETOXIFICATION OF REACTIVE OXYGEN SPECIES IN BIOLOGICAL SYSTEMS. ( Clark et al., 1986) 0; L-- .v,,%!Gq O? ' - ,Fez' GSH GSSG - h-+* t 616 'qbi2 -Fe3' i hot4 CELL TOXICITY Superoxide GSH-PX - glutathione peroxidase SOD - Superoxide dismutase GR - Qlutahone reductase GSH - reduced glutathione .OH - hydroxyl radical GSSG - oidised glutathtone S - secondary radical
1973). The two major systems <strong>of</strong> LPO are non-enzymatic ascorbate induced system (Ottolenghi, 1959) and enzymatic NADPH induced system (Hochstein and Enister, 1963) mediated by NADPH cytochrome-c-reductase. Substances such as ascorbate and ferrous ions, which induce ~e" to ~e", and peroxides enhance LPO (Halliwell and Guaeridge, 1989). LPO decreases membrane fluidity, increases leakiness <strong>of</strong> <strong>the</strong> membrane (Jacob and Lux, 1968) to substances that are normally impermeable, inactivates membrane bound enzymes (Kesner et a/., 1979) along with <strong>the</strong> fatty acid and antioxidant depletion. Damage to <strong>the</strong> membrane may be subtle and involve only small changes in <strong>the</strong> composition <strong>of</strong> fatty acids, yet <strong>of</strong>ten sufficient to greatly increase <strong>the</strong> susceptibility <strong>of</strong> <strong>the</strong> membrane to oxidative damage (Halliwell and Guneridge, 1985). Oxygen radicals are generated inside leucocytes enabling <strong>the</strong>m to kill phagocytosed microorganisms (Babior el al., 1973). Unfottunately for <strong>the</strong> host, <strong>the</strong>se leucocytes can also secrete superoxide radicals along with o<strong>the</strong>r mediators from <strong>the</strong>ir outer membrane into <strong>the</strong> surroundings (Nathan and Root, 1977). This indiscriminate and self-inflicting process contributes to <strong>the</strong> tissue damage or inflammation (Fig. 54) (Fantone and Ward, 1982; Weiss and LoBuglio, 1982; Fteeman and Crapo, 1982) and has <strong>the</strong> capacity to cause tissue damage in <strong>parasite</strong> induced disease. Johnson and Ward (1982) reponed that <strong>the</strong>se events occur much more vigorously when certain receptors on <strong>the</strong> surface <strong>of</strong> leucocytes, such as those responsible to antigen-antibody complexes (Fc receptors) and to complement components are activated. Thus endo<strong>the</strong>lial damage in he rat, ~nitiated by immune complexes or C5 activation, can be prevented by depleting animals <strong>of</strong> neutrophils (Till er al., 1982), infusing SOD or catalase (Johnson and Ward, 1981; McCormick er a!.. 1981). radical scavengers (Ward er al., 1983% Fligiel era/.. 1984; Fox 1984) and iron chelators (Ward ef al., 1983b). Baba ef al. (1989) reported that, in M. nalalensis infected with D. vileae, <strong>the</strong>re was increase in LPO in <strong>the</strong> organs such as liver and spleen and decrease in lungs. Red blood cells infected with P. bwghei have been observed to show five-fold increase in LPO than <strong>the</strong> normal (Etkin and Eaton, 1975). Mahdi et a/. (1992) reported increased levels <strong>of</strong> lipid Wxid~~ in brain <strong>of</strong> M. natalemis infected with P. berghei. Elevated levels <strong>of</strong> LPO products during malarial <strong>infection</strong> had been reported (DesCamps er a1.,,1987; Nalr ef al., 3
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EFFECT OF INFECTION OF THE FILARIAL
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I wish to express my deep sense of
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1. INTRODUCTlON 2. REVIEW OF LlTERA
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As stated earlier, the host immune
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433 DISCUSSION Testosterone is a se
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CHAPTER 4.4 HISTOPATHOLOGICAL CHANG
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Platc 2 Plate 3 Plate 4 Plate 5 Pla
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Platc X Plate 9 Plate 10 Plate 11 P
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Plate w: Section of Testes of norma
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4.4.2.1.5 Brain The control animals
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Plate ICt Section of Kidney of infe
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4.4.2.2 Histopathological changes i
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Plate 32
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The mf could not be seen in spleen
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ain, it decreased from 0 day itself
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inflammatory nature indicative of c
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BIBLIOGRAPHY Ackerman, S.J., Gleich
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Case, T., Leis, B., Witte, M., Way,
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Drabkin, D.L.R. and Austin, J.H. (1
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Fukuota, M., Zhou, Y. and Tanaka.(l
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Jacob, H.S. and Lux, S.E. (1968). D
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Linda, I. and Mayeda, B. (1974). Th
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Murray, H.W. (1981). Susceptibility
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Santiago- Stevenson, D., Oliver-Gon
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Tate, S.S., Thomson, G.A. and Meist
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Zaini, M., Ramachandran, C.P. and E