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

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the period by which, the parasite attains full development and gets lodged in the organs. In lungs, conhary to other'organs, the levels of SOD and catalase showed increasing trend throughout the study period indicating that more amount of NADPH is formed by the restoration of G6PDH (sa. 4.1.2.1.6), even though the parasite burden is higher than that observed in other organs. The activity of SOD and catalaw which were altered in all the organs of B.ma1ayi infected animals were restored to normal levels after DEC treatment. And this may be associated with concornittarit generation of NADPH by the increase in G6PDH activity after DEC treatment as observed (sec. 4.1.2.3.2). 4.133 Glutathione and glutathione related enzymes GSH plays an important role in protection of cells against oxidants in most organisms (Bryant and Behm, 1989). Depletion of GSH leads to lethal conditions and accumulation of oxidii glutathione (GSSG), which is also harmful to cells, because it forms mixed disulphides with proteins and other molecules containing thiol groups. The concentration of GSH in tissues is regulated by its generating enzyme GR from oxidised glutathione. The utilising enzymes GPx and GST convert the reduced state (GSH) to oxidized form (GSSG) during the detoxification of the radicals. The NADPH reqd for GR activity is regenerated by the enzyme G6PDH (Halliwell and Gutteridge, 1990). Jakoby et al. (1976) reported that GSH is capable of protecting cells from oxidant stms owing to its antioxidant and nucleophilic charactenstics. It helps in maintaining the integrity of nd cells (Fegler. 1952) particularly when exposed to oxidant stress due to drug or malarial infection (Allen and Jandl, ]%I) by protecting hemoglobin and other thiol containing proteins from denaturation. GPx plays an important role in the detoxificat~on of Hz&, organic hydroperoxides or lipid peroxides (Cohen and Hochstein, 1963: Chnstopherson, 1%8; 1969; Flohe, 1982). GSH and NADPH are required in awuate amount for GPx activity @*their depletion.
esults in its reduced activity (Condell and Tappell, 1983). Also that GPx is inactivated under severe oxidative sees^. . In P. knowlesi infected monkey, the activity of GSH had been reported to be decreased (Fulton and Grant, 1956; Fletcher and Maepith. 1970). Bhattacharya and Swarupmithra (1987) reported a decline in the etythrocyte GSH In P.vivlu infected patients. P. knowlesi infection resulted in elevation of hepatic stress in monkeys, besides affecting the antioxidant enzymes of the host. Gpx activity was found to be low in P. vinckei infected mice erythrocytes by Stocker et al. (1985) and in P. viva by Mathews and Selvam (1993) and Sarin (1 993). In studies with P. falcipanrm and P. viva infected RBC's GR activity was also found to be reduced (Stocker et al., 1985; Kamchogwongpaisan el al., 1989). Litlov el al. (1981) reported that in the absence of GSH, loss of GR activity is seen. GST is one of the GSH utilizing enzymes and reduction in GSH leads to the decreased activity of GST (Srivastava el al., 1995). Picard- Maureau er al. (1975) had observed decrease in the activity of G6PDH of P.vinckei parasitized mice erythrocytes and a similar trend was reported in P. bergei infected mice (Nair et 01.. 1984; Grindberg and Soprunov, 1983) and in the RBC's of patients afflicted w~th malaria (Mathews er al., 1991). Srivastava er al. (1991; 1992) and Clark et al. (1986; 1989) reported an increased oxidative damage during malaria infection and attributed this to decreased GST level. Srivastava er al. (1995) had shown that P berghei infection in M.naraletzsis reduced the activity of GST in the hepatic mitochondria and microsome and the GST level was brought back to normal aAer chloroquine treatment. Mathews and Selvam (1993) reported decreased GST activity in P. vivor infected human erythrocytes. In the present study, GSH level decreased in liver, brain, testes and heart of the B,mafayi infected animals, but in lungs it showed an increasing trend. A negative correlation was observed between the activity of GSH and LPO in all the organs (Figs. 70-74) and it was significant w0.05) in liver (I=-0.88), testes (I=-0.95) and heari (r--0.88) only. Similarly a positive cornlation was observed between the activity of GST and GSI~ ip all the organs
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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
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the compound kills the filarial wor
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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 and 70: 1 - 0- ' 1 5 - 6 - 7 - Fig.63:Relat
Page 71 and 72: Catalase had been reported to be re
Page 73: - Fig.68:Relationship between chang
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
Page 121 and 122: Plate w: Section of Testes of norma
Page 123 and 124: 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
Page 159 and 160:
Zaini, M., Ramachandran, C.P. and E
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