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

1981), and their increase in human patients with P.falciparum infection are associated with
complications and death. P. vinckei infected RBCs have also been reported to generate
significant levels of malondialdehyde (Clark et al., 1984a, b; Stocker et al., 1985) and it has
been suggested that LPO can be set into motion whenever conditions of increased oxidative
stress or decreased antioxidant defences occur in the cell.
Production of reactive oxygen species in mice infected with P. berghei and P. yeolii
had been reported (Li and Li, 1987; Dockrell and Playfair, 1984). It has been suggested that
HI@ and the reactive oxygen radicals from the respiratory burst have the potential to initiate
LPO, resulting in the formation of toxic aldehydes. Clark ei al. (1987) reported that products
of LPO are toxic and inhibitory against malarial parasite P. falcipam. The products of
macrophage secretions such as oxygenderived free radicals and tumour necrosis factor are
shown to kill the human malarial parasite P. falciparum invitro (Worncraft er al., 1984) and
also initial stages of P. berghei in rodents (Wozencrafl et al., 1985). Hydrogen peroxide
injected intravenously caused a drop in parasitaemia in mice with P. yeolii or P. chaubadi
and can kill P. yeolii and P, berghei maintained invifro (Dockrell and Playfair, 1983). Gharib
et al. (1999) reported a two fold increase in LPO and decreased antioxidants at the site of
pulomatous inflammation in liver infected with Schistosoma mansoni.
ln the present study, it has been found that following infection of B.malayi, LPO
was sigruficantly high in liver, testes, brain and heart of M.natalemis, whereas in lungs it
was low. A negative correlation was observed between the LPO and activity of SOD1
catalase in liver, testes, brain and heart (Figs.55-58, 60, 62-64) and the correlation was
significant 0 .05) in liver (SOD I= -0.96). testes (SOD r= -0.97), Brain (catalase -0.89)
and heart (catalase r--0.92) only. The LPO levels, on the contmy, had a positive correlation
with catalase in testes and with SOD in lungs, however it was significant in the lungs (SOD
r= -0.88, p4.05) only (Figs. 59 & 61). This increase in LPO is due to the decrease in the
antioxidant caqmcs and GSH production in these organs. But in lungs LPO operates below
the normal level, although superoxide anions may be produced at a greater rate than in
control, it however, appears to be removed by elevated SOD and catalase (sec. 4.1.2.1.1
Br4.1.2.1.2).