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

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The LPO altered during infection of B.malayi was brought back to normal levels after DEC treatment and this has happened due to the restoration of the activity of antioxidant enzymes and GSH to normal levels as observed in a further experiment. In testes, the LPO was remarkably high compared to controls and even after DEC treatment, did not reach normal level. This may be due to the irreversible tissue damage as evidenced in histopathological studies (sec. 4.4.2.2). 4.1.3.2 Superoxide dismutase and catalase The cells are rich in the antioxidants such as GSH and an antioxidant enzyme like catalase, SOD. GR and GPx and contains a proteolytic system that can hydrolyze oxidatively modified protein (Halliwell and Gutteridge, 1989). Disrnutation of superoxide anion is catalysed by SOD, which yields Hz@, and it is Wer decomposed by the enzyme catalase and glutahone peroxidase. This reaction plays a major role in protecting the cell membrane from H2q (Jacob er a/., 1%5; Panicker and Zyer, 1969), but a decrease in the activities of SOD, catalase. GPx, GR and GSH level can exacerbate LPO. Studies conducted on D.viteae infected animals (Baba et a/., 1989), indicated that the act~vity of SOD decreased in liver and spleen, but increased in lungs. Red blood cells parasitized by P.krghei (Fairfield et a/.. 1983; 1986) and P. vinckei (Stocker et al., 1985) contained less SOD and catalase than the RBC's of uninfected. Altered levels of SOD have also been nponed in patients with P. falcipanun mfection and in mice with P. berghei and P. vinckei infection (Areekul and Boonme, 1985, 1987; Suthipak el nl., 1982; Stocker et al., 1985; Fairfield el a/., 1988). Areckul and Boom (1987) had shown that higher parasitaemia of RBC's, due to Pjalcipnun is associated with higher SOD activity compared to the uninfected ones. Fairfield et a/. (1983) reported that P. berghei devoid of endogenous SOD adopts e yhqte SOD for protection against the deleterious effect of superoxide radicals and consequently reduces the host SOD level. SOD and catalase were decnesed significantly in P, v im malaria in patients (Mathews and Selvam, 1991). SOD showed restoration of enzyme activity while. catalase activity was increased significantly after primaquine trratmcnt.
Catalase had been reported to be responsible for the detoxification of Hz@ (Brenner and Alison, 1953; ~icholis, 1965). Small quantity of erythrocyte catalase was observed to exist in inactive form viz., catalase complex I1 (Leibowitz and Cohen, 1968). The conversion of complex I1 to active form is dependent on the reducing agent NADPH (Eaton el al., 1972). Under conditions of increased oxidative stress, it is likely that more NADP rather than NADPH is formed, which is required for the activation of catalase. The decreased NADPH and G6PDH leads to reduced catalase activity (Eaton er al., 1972). The reactive oxygen radicals can also inhibit the activity of catalase and GPx as had been observed by Hodgson and Fridovich (1975) and Searle and Wilson (1980). In M nalulensis infected with D. viteae, decreased activities of catalase and xanthine oxidase and increased LPO were observed in liver and spleen (Batra el al.. 1989). And on the other hand, in lungs the elevated activity of xanthine oxidase and catalase prevented the LPO. Catalase activity was also found to be low in P, vivm (Mathews and Selvam, 1991) and P. ful~ipanun (Areekul and Boonme, 1987) infected human erythrocytes, and in mrce erythrocytes infected with P. berghei (Nair e! al., 1984) and P. Vinckei mckard- Maureau el al.. 1975). In the pment study, in the liver, brain, testes and heart of the infected animals, the actlvrty of catalase increased initially and declined later. However, in lungs, its activity rncreased wrth the propion of the parasite development. Fielden et al. (1974) and Bray (1974) observed that SOD activity never decreased in the presence of catalase, which suggested that the reaction product H 2q inactivated SOD (Yamakura and Suzuki, 1986). Kono and Fridovich (1982) demonsmted that catalase was inhibited by superoxide anion and concluded that SOD and catalse are mutually acting protective set of enzymes. In the present study, a positive correlation was obsewed between the activity of SOD and catalase In liver, brain. heat and lungs (Figs. 65,67-69), and the relationship was significant w0.05) In brain (14.94) and heart (~0.97) only. Compared to this, in the testes, a negative cornlation was observed Ween the activity of SOD and catalase, and it was not significant. The deed SOD and catalase activity in the organs of B. malayi infected animals may be due to the inhibition by reactive oxygen radicals released and non- availability of NADPH. This is &m~ed between 60 and 120 days post rnfection, which is &
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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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13 Testicular changes Testosterone
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2. REVIEW OF LITERATURE Filariasis
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2.2 Clinical signs Inflammalation o
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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 and 64: 1973). The two major systems of LPO
Page 65 and 66: 1981), and their increase in human
Page 67 and 68: 1 0 Fig.58:Relationship between cha
Page 69: 1 - 0- ' 1 5 - 6 - 7 - Fig.63:Relat
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
Page 117 and 118: Platc 2 Plate 3 Plate 4 Plate 5 Pla
Page 119 and 120: 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
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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