effect of infection of the filarial parasite brugia malayi - Pondicherry ...

1973). The two major systems of 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 of the membrane (Jacob
and Lux, 1968) to substances that are normally impermeable, inactivates membrane
bound enzymes (Kesner et a/., 1979) along with the fatty acid and antioxidant depletion.
Damage to the membrane may be subtle and involve only small changes in the
composition of fatty acids, yet often sufficient to greatly increase the susceptibility of the
membrane to oxidative damage (Halliwell and Guneridge, 1985).
Oxygen radicals are generated inside leucocytes enabling them to kill phagocytosed
microorganisms (Babior el al., 1973). Unfottunately for the host, these leucocytes can also
secrete superoxide radicals along with other mediators from their outer membrane into the
surroundings (Nathan and Root, 1977). This indiscriminate and self-inflicting process
contributes to the tissue damage or inflammation (Fig. 54) (Fantone and Ward, 1982; Weiss
and LoBuglio, 1982; Fteeman and Crapo, 1982) and has the capacity to cause tissue damage
in parasite induced disease. Johnson and Ward (1982) reponed that these events occur much
more vigorously when certain receptors on the surface of leucocytes, such as those
responsible to antigen-antibody complexes (Fc receptors) and to complement components
are activated. Thus endothelial damage in he rat, ~nitiated by immune complexes or C5
activation, can be prevented by depleting animals of 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, there was
increase in LPO in the 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 the
normal (Etkin and Eaton, 1975). Mahdi et a/. (1992) reported increased levels of lipid
Wxid~~ in brain of M. natalemis infected with P. berghei. Elevated levels of LPO
products during malarial infection had been reported (DesCamps er a1.,,1987; Nalr ef al.,
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