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

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Fig.93:Relationship between change In GPx and GSH levels in heart 61 1 5- 4- 1 3- (I) 0 2- 1 - 0- 1 - 0 y=-0 41 +O 79.x 1 2 3 4 5 6 GPx I Observed values + Expected values I Fig.94:Relationship between change in GPx and GSH levels in lungs , --A -0 5 0 0 5 1 15 2 2 5 3 GPx I Obse~ed values - Expected values I
A reduction in the total thiol contents was observed in the present study in different organs of B.malayi infected animals. A significant w.05) positive comlation was observed between thiol status and GSH levels in all the organs (Figs. 95-99) such as liver (d.96), testes (~0.9). brain (~0.98). heart (r=0.96) and lungs (I4.89). (Kosower et al. (1982) had shown a direct link between the thiol status of the membrane and cellular GSH. This shows that the function of GSH is to serve as a reducer of membrane protein disulphides and to avert membrane thiol oxidation. The decreased GSH concentration observed in the present study had contributed to decreased thiol status, while in lungs the availability of GSH had increased the thiol level. The decreased total thiol levels in the B.malayi infected animals were restored to the normal levels after DEC therapy, which is due to the restoration ofGSH levels (sec. 4.1.2.3.2). 4.13.5 Ascorbic acid The antioxidant property of ascorbic acid is often associated with its ability to regenerate vitamin E h m vitamin E radical (Niki eta/., 1984). Nishlkimi (1975) had shown that ascorbate reacts with superoxide and converts it to Hz@. Ascorbic acid levels in plasma were found to be decreased due to P.vivar infection (Irwin and Hutchins, 1976; Frei er a/., 1988). Tappel (1969) and Grimble and Hughes (1967) reported that GSH is required for the conversion of dehydroascorbate to ascorbate. In the present study ascorbic acid levels were found to be low in liver, brain, testes and heart except for lungs of the B.malayi infected animals, which is due to the alteration in GSH level during infection. The ascorbic acid level and GSH had positive comlation in all the organs (Figs. 100-104) and it was significant w0.05) in liver (r=0.99), testes (~0.89)~ brain (r= 0.88) and heart (14.97) only. And the restoration of the ascorbic acid levels observed in the infected animals after DEC treatment is due to the restored GSH levels (sec. 4.1.2.3.2).
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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
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Ragenb 1. Tris-HCI buffer . : 0.1 M
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3. Reduced glutathione : 30 mM To I
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4.1.1.6 Glucose-6-phosphate dehydro
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absorbance of the clear supernatant
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-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 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: V) (3 :; - Fig.9O:Relationship betw
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
Page 126 and 127: Plate ICt Section of Kidney of infe
Page 128 and 129: 4.4.2.2 Histopathological changes i
Page 130 and 131: Plate 32
Page 132: The mf could not be seen in spleen
Page 135 and 136: 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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