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

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801 70 - 0, - 3 60m > 50- 40- Fig. 1 1 2: Effect of 8. malayi on Lymphocytes of M.natalensis 90 -, 1 30- 20 - 10- E 0 0 30 60 90 120 Days of infection Fig.113: Effect of B. malayi on Neutrophils & Eosinophils in Mastomys 7" 40 - 35- 0, - 3 30m > 25- 20" 4B 5 15- 10- 5- - -. OF 0 30 60 90 120 Days of infection -
efflux and thereby alter the membrane permeability, and also likely to affect the transport of Na' ions as well as nerve impulses and synaptic functions of the brain as reported above. The decrease in ca2' ATPase and Mg2' ATPase activities is due to peroxidation of the membrane lipids (sec 4.1.2.2). The lowered activity of Mg2' ATPase and ca2' ATPase observed in the B, molayi infected animals is bound to alter the permeability of the CNS membrane, and cause disturbances in the concen!mtion of ~ g and " ca2'. The decreased acetylcholinesterase activity in the present study may be due to altered lipid fluidity of the CNS membrane because of peroxidation (Howard and Sawyer, 1980). yGTP is an extrinsic membrane glycoprotein (Tate and Meister, 1976) widely distributed in kidney, brain and liver. Brain endothelial cells are also rich yGTP and alkaline phosphatase, which are responsible for transendothelial hansport and vascular permeability (Vorbrodt el al', 1986). Tripathi er a/. (1994) reported a decrease in the yGTP and atkalie phosphatase activity in the cerebral microcapillaries of mice infected with P. yoelii. In the present study, the decrease in y-GTP and alkaline phosphatase due to B.mnlnyi infection indicates membrane damage in the brain. The increased LPO (section 4.1.2.2) may be responsible for the membrane damage of the brain cells. Moreover, the decrease in ahkine phosphatase and y-GTP and acetylcholinesterase may increase disruption in blood brain barrier permeability and lead to abnormal cerebral metabolism. 4.23.2 Membrane bound enzymes of RBCs. Oxygen radicals cause more damage to red cells than to other cells, since they are exposed to high oxygen concentrations in the lungs. The red cell membrane contains unusually high concentration of vulnerable unsaturated fatty acids and lacks the cytochrome respiratory pathway, which allows most of the oxygen in other cells to avoid sequential acquisition of electrons (Suhail and Rizvi, 1990). Thus, reactive forms of oxygen are generated at a higher rate in red cells and the balance between this stress and their antioxidant defmces determines their life span (Carrel et al., 1975). Mice red cells infected with P. vinckei had been reported to d9)age the membrane calcium hansporl system due to the accumulation of rnalondialdehyde (Kayen ef al., 1983),
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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
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4.1.2.1 Changes in antioxidant enzy
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Fig.3: Effect of B.malayi on SOD in
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Fig.9: Effect of B.rnalayi on GST i
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Fig.12: Effect of 6.rnalayi on GPx
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Fig. 18: Effect of B.malayi on G6PD
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12- 3 m- 15- lor, Fig.21: Effect of
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Fig.27: Effect of B.malayi on Ascor
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4.1.2.3 Change in the antioxidant e
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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 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: - Fig.110: Effect of 6. malayi on H
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
Page 137: inflammatory nature indicative of c
Page 141 and 142: BIBLIOGRAPHY Ackerman, S.J., Gleich
Page 143 and 144: Case, T., Leis, B., Witte, M., Way,
Page 145 and 146: Drabkin, D.L.R. and Austin, J.H. (1
Page 147 and 148: Fukuota, M., Zhou, Y. and Tanaka.(l
Page 149 and 150: Jacob, H.S. and Lux, S.E. (1968). D
Page 151 and 152: Linda, I. and Mayeda, B. (1974). Th
Page 153 and 154: 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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