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

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FIG. 54 THE SEQUENCE OF EVENTS IN FREE RADICAL MEDIATED LIPID PEROXIDATION (FANTONE AND WARD, 1982) R'+ PUFA -+ PIJFA'. R initialion phase puFi.oi -> PROTEIN (- propagation l'l'i A scavenger' WFA.OH. H,O henc conjugates malonyld~aldchydr crhanc penlanc phase Free & ~ Q~ndude S reduced glutahon+ other hols (for mple, protan hols). vitunin $ d ud flat em^ Scavepyg auyim include supmade htase, -dBkuat~av=
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).
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EFFECT OF INFECTION OF THE FILARIAL
Page 4 and 5:
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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13 Testicular changes Testosterone
Page 14 and 15: 2. REVIEW OF LITERATURE Filariasis
Page 16 and 17: 2.2 Clinical signs Inflammalation o
Page 18 and 19: the tegument by the release of thei
Page 20 and 21: the compound kills the filarial wor
Page 22: 3. MATERIALS AND METHODS COLONY MAI
Page 25 and 26: Ragenb 1. Tris-HCI buffer . : 0.1 M
Page 27 and 28: 3. Reduced glutathione : 30 mM To I
Page 29 and 30: 4.1.1.6 Glucose-6-phosphate dehydro
Page 31 and 32: absorbance of the clear supernatant
Page 33 and 34: -eats I. Lowry's reagent :Solution
Page 35 and 36: 4.1.2.1 Changes in antioxidant enzy
Page 37 and 38: Fig.3: Effect of B.malayi on SOD in
Page 39 and 40: Fig.9: Effect of B.rnalayi on GST i
Page 41 and 42: Fig.12: Effect of 6.rnalayi on GPx
Page 43 and 44: Fig. 18: Effect of B.malayi on G6PD
Page 45 and 46: 12- 3 m- 15- lor, Fig.21: Effect of
Page 47 and 48: Fig.27: Effect of B.malayi on Ascor
Page 49 and 50: 4.1.2.3 Change in the antioxidant e
Page 51 and 52: Fig.35: Effect of B.malayi on CAT i
Page 53 and 54: m 20 0) - 15 9 g 10 il! 5 0 Fig.39:
Page 55 and 56: 30 25 8 - a 20 2 15 C I 10 I 5 0 35
Page 57 and 58: Fig.45: Effect of B.maiayi on GSH i
Page 59 and 60: Fig.49: Effect of B.malayi on Vit-C
Page 61 and 62: 4.1.3 DISCUSSION 4.1 3.1.1 Toxic ox
Page 63: 1973). The two major systems of LPO
Page 67 and 68: 1 0 Fig.58:Relationship between cha
Page 69 and 70: 1 - 0- ' 1 5 - 6 - 7 - Fig.63:Relat
Page 71 and 72: Catalase had been reported to be re
Page 73 and 74: - Fig.68:Relationship between chang
Page 75 and 76: esults in its reduced activity (Con
Page 77 and 78: g 20- :I-. F1g.70:Relationship betw
Page 79 and 80: 12, - I 0 U) Q 4 2 0 - + - Fig.75:R
Page 81 and 82: $ Fig.80:Relationship between chang
Page 83 and 84: Fig.85:Relationship between change
Page 85 and 86: V) (3 :; - Fig.9O:Relationship betw
Page 87 and 88: A reduction in the total thiol cont
Page 89 and 90: 2 5- Fig.98:Relationship between ch
Page 91 and 92: Fig. 103:Relationship between chang
Page 93 and 94: 4.2.1.1 N ay ATPase Reagents Nay AT
Page 95 and 96: Reagents 1. Acetylcholine bromide :
Page 97 and 98: To 1.5 ml of carbonate buffer, 1.5
Page 99 and 100: 4.2.1.10 Differential leucocyte cou
Page 101 and 102: increase in the control animals (Fi
Page 103 and 104: - Fig.110: Effect of 6. malayi on H
Page 105 and 106: efflux and thereby alter the membra
Page 107 and 108: with i n d lymphocytes and decrease
Page 109 and 110: Tubes were labeled for calibrators,
Page 111 and 112: Fig.114: Effect of B, malayi on GTP
Page 113 and 114: 433 DISCUSSION Testosterone is a se
Page 115 and 116:
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
Page 147 and 148:
Fukuota, M., Zhou, Y. and Tanaka.(l
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Jacob, H.S. and Lux, S.E. (1968). D
Page 151 and 152:
Linda, I. and Mayeda, B. (1974). Th
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Murray, H.W. (1981). Susceptibility
Page 155 and 156:
Santiago- Stevenson, D., Oliver-Gon
Page 157 and 158:
Tate, S.S., Thomson, G.A. and Meist
Page 159 and 160:
Zaini, M., Ramachandran, C.P. and E
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