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

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thereby increasing intracellular calcium. Tanabe et al. (1983) have shown reduced ca2' ATPase and M~Z' ATPase in P, chaubadi cells. They had also reported that the Nay ATPase activity of the host cell membrane was 85% less than the normal. So the permeability changed due to decreased ATPase, which would have resulted from the membrane lipid changes in the RBC The observed decrease in N~-K' ATPase, ca2' ATPase and M~~ ATPase and acetylcholinesterase activity in RBC in the present study indicates membrane damage. The reduction in the activity of ATPases can be explained from the fact that they are lipid and thiol dependent enzymes. and their decreased activity can be attributed to membrane damage as reported above. Decrease in ca2* ATPase and M ~ ATPase ~ ' activity may be due to peroxidation of the membrane lip~ds. The erythrocyte membrane is normally less permeable to extracellular Ca2'. Enhanced host membrane permeability to Ca2+ is combined with reduced activity of Ca2' ATPase, leading to an increase In intracellular ca2' (Sarkadi, 1980). Acetylcholinesterase is an erythrocyte specific enzyme (Mitchell el al., 1965). Elevated cholinesterase in mouse erythrocytes infected with P. chaubadi (Konigk and Mitsh, 1977), and P. berghei (Areekul and Cheerarnakara, 1987) had been reported. The decrease in acetylcholinesterase in 5. malayi infected animals may be due to altered lipid fluidity of the cell membrane (Howard and Sawyer. 1980). 4.233 Haematological parameters Butteworth (1977) and Ogilvie et al. (1978) observed changes in the absolute count of neutmphils. lymphocytes. monocytes and granulocytes in helminthic mfection. Choong and Mak (1991) reported an increase in total count, differential counts and blood eosinophils to k times at 3 weeks post infection upto 13 weeks in Presbytis cristata infected with 5. Malayi. It further increased to five tims upto 20 weeks, but no change in total leucocyte count was observed. An increase in neutrophils was reported in Toxoplasma mfection (Frcnkel. 1973). Rahmah el 01. (1994) reported that Toxoplarma gondi infection resulted in the increase in neutrophils and cosinophils and a decrease in lymphocytes. Larsh (1967) and Cypas ( 1972) reported infection of mice by Trichinella spimlir and Nematospiroides dubia
with i n d lymphocytes and decreased neutrophils. In P. viva and P. falcipamm infection, decreased lymphocytes, increased monocytes and eosinophils had been observed without significant changesin total leucocyte, neutrophil and platelet counts (Kurnaresan and Selvam, 1991). Eosinophils and neutrophils play a significant role in host defense against the parasites. In Onchocerciasis infections, eosinophils were shown to be the major participants in adherence to 0. wlvulus (William er al., 1987). The cationic proteins of the eosinophil damage target cells through membrane interaction, since the major basic protein as well as eosinophil cationic proteins can disrupt cell membrane. Mackenzie (1980) had shown that eosinophils eventually target mf and Greene er 01. (1981) had shown that neutrophils are equally efficient in the same system. In the present study the haernoglobin levels and RBC counts were not altered due to the B. mnloyi mfection, while total WBC counts showed a decrease below nonnal values. The significant increase in neutmphil and eosinophil counts and decrease in lymphocytes confirm the above findings.
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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
Page 11 and 12:
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
Page 33 and 34:
-eats I. Lowry's reagent :Solution
Page 35 and 36:
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
Page 45 and 46:
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
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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 and 104: - Fig.110: Effect of 6. malayi on H
Page 105: efflux and thereby alter the membra
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
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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