Released August 2007 - The Indian Society for Parasitology

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32Sangwan et al.function of copper has been suggested (Suttle et al., levels of ATP-synthase and cytochrome C oxidase subunit1987). On the basis of above findings, anaemia can not peptide from hearts of copper deficient rats are not alteredbe due to iron deficiency as liver iron concentration by the administration of dimethyl sulphoxide. J Nutrition24:789-903.was normal and indicated the failure in properutilization of Fe for Hb synthesis as infected animals Cousins RJ. 1985. Absorption, transport and hepatichad significantly low levels of copper in their tissues metabolism of copper and zinc: special reference toand plasma. Also, in an earlier study (Sangwan et al., metallothionein and caeruloplasmin. Physio Reviews65:238-296.1993), significantly low levels of folacin andcobalamin have been reported in buffaloes suffering Evans P and Halliwell B. 2001. Micronutrient:from T. evansi, which might have additionally oxidant/antioxidant status. British J Nutrition 65 suppl.contributed to the further reduction in Hb synthesis as S67-S74.these two vitamins are involved in maturation and Gill BS. 1991. Trypanosomes and Trypanosomiasis of Indiandevelopment of erythrocytes. So, in addition to Livestock. Publications and Information Division, ICAR,folacin and cyanocobalamin, copper deficiency may PUSA, New Delhi. pp 192.also be contributing to the development of anaemia in Gross AM and Prohaska JR. 1990. Copper deficient mice havetrypanosomosis, and iron is not the limiting factor for higher cardiac epinephric turnover. J Nutrition 120:88-96.the development of anaemia in the infected animals as Henle ES and Linn S. 1997. Formation, prevention and repairis the general view about this disease (Mwangi et al., of DNA damage by iron/hydrogen peroxide. J Bio Chem1995). 272:19095-19098.Saneko EL, Yaroplov AI and Harris ED. 1994. Biologicalfunctions of caeruloplasmin expressed through copper-binding sites. J Trace Elements and Exp Med 7: 69-88.Iron deficiency could also be indicated by low levelsof iron in liver and a marginal band of 150–250 mg/kgdry matter is tentatively proposed to separate thedeficient from the normal. However, in the presentstudy, liver and spleen iron values were reduced butnot to the extent that anaemia may develop. It is opinedthat it is the deficiency of copper, and not of iron, to bethe major factor responsible for the development ofanaemia and other clinical symptoms in rabbitssuffering from T. evansi infection. This study has alsohelped in understanding the pathophysiology ofmetal-ions in trypanosomosis, and the properremedial measures like copper supplementationshould be introduced to reduce the convalescentperiod by providing suitable supportive treatmentmeasures.ACKNOWLEDGEMENTSThis work was done at CCS Haryana AgriculturalUniversity, Regional Research Station, Uchani,Karnal, and financially supported by the NationalAgricultural Research Project of the Indian Council ofAgricultural Research, New Delhi.REFERENCESAvasathi BL, Kathuria IG and Parjapati KS. 1985. Course ofinfection in rabbits experimentally infected withTrypanosoma evansi. Indian J Parasitol 9:281-282.Chand K and Singh RP. 1971. A study on the clinical course oftrypanosomiosis in goats, donkeys, dogs and rabbitsexperimentally infected with Trypanosoma evansi. J Res8:270-274.Chao JCJ, Medeiros DM, Davidson J and Shiry L. 1994. LowKreier JP. 1977. Parasitic Protozoa. Vol. I Academic Press, NewYork, San Francisco, London. pp 277-288.Radostits OM, Gay CC, Blood DC and Hinchcliff. 2000.Veterinary Medicine. Ninth Ed. W.B. Saunders CompanyLtd., London. P. 1335.Monzon CM and Villavicencio VI. 1990. Serum proteins inguinea pigs and horses infected with Trypanosoma evansi(Steel, 1885). Vet Parasitol 36:295-301.Mwangi SM, McOdimba F, Logan-Henfrey L. 1995. The effectof Trypanosoma brucei brucei infection on rabbit plasmairon and zinc concentrations. Acta Tropica. 59:283-291.Sangwan N, Chaudhri SS, Rao AR, Sangwan AK and Gupta RP.1993. Folacin and cyanocobalamin in relation to naturalTrypanosoma evansi infection in buffaloes. Trop AnimalHealth and Production. 25:79-84.Schalm OW, Jain NC and Caroll EJ (Eds.). 1975. VeterinaryHaematology. Third ed., Lea and Fabiger, Philadelphia.Snedecor GW and Cochran WJ.1967. Statistical Methods:Seventh ed. Oxford and IBG Publishing Co., New Delhi.Suttle NF, Jones DG, Woolliams C and Woolliams JA. 1987.Heinz body anaemia in lambs with deficiencies of copperand selenium. British J of Nutrition 58:539-548.Underwood EJ and Suttle NF. 1999. The Mineral Nutrition ofLivestock. Third ed. CAB International Publishing Co. pp312, 361.Williams DM, Kennedy FS and Green BG. 1983. Hepaticiron accumulation in copper-deficient rats. British J ofNutrition. 50:653-660.
Journal of Parasitic Diseases: June 2007, Vol. 31, No. 1, 33-37Original paperJ P DGlutathione synthetase in Plasmodium bergheiS. K. Sharma and H. S. BanyalDepartment of Biosciences, H. P. University, Shimla.Received 1 August 2006; revised 7 May 2007; accepted 22 May 2007ABSTRACT. Cell-free Plasmodium berghei (NK-65) contained 5.6-times more (around0.443±0.001 U/mg protein) glutathione synthetase (E.C. 6.3.2.3) enzyme activity as compared tonormal mouse erythrocytes. Subcellular fractionation revealed that enzyme activity is mainlyconfined to the cytosolic part of parasite. Around 41-fold purification of enzyme was achieved byusing a combination of ammonium sulphate fractionation and Sephadex G-200 gel filtration. Thepurified enzyme had a molecular weight of 70 kDa.Keywords: cell-free parasite, erythrocytes, glutathione, glutathione synthetase, PlasmodiumbergheiINTRODUCTIONand glutathione synthetase (GS). GS (γ-L-glutamate-L-cysteine: glycine ligase, E.C. 6.3.2.3) catalyzes theThe ubiquitous tripeptide glutathione (L-γ-glutamyl- ATP-dependent conversion of dipeptide γ-L-cysteinylglycine; GSH), usually the most prevalent glutamylcysteine to glutathione.intracellular thiol, is known to function directly orindirectly in many important biological phenomena GS was first demonstrated by Snoke and Bloch (1952)including synthesis of proteins and DNA, their in pigeon liver extracts and showed γ-transport, enzyme activity, metabolism and protection glutamylcysteine, an intermediate in the synthesis ofof cells against oxidative stress (Anderson et al., 1985; glutathione. The enzyme has subsequently beenSies, 1989). Plasmodium species invade and survive studied in Escherichia coli (Samuels, 1953), yeastinside erythrocytes by overcoming the stress exhibited (Mooze and Meister, 1967), human erythrocytesby the host cell. In malaria parasite, pathways for (Majerus et al., 1971), rat kidney (Oppenheimer et al.,detoxification of xenobiotics, antimalarial drugs and 1979) and P. falciparum (Meierjohann et al., 2002).maintenance of intracellular reducing environment Characterization of E. coli GS has demonstrated thatrely on glutathione (Becker et al., 2003; 2004). All the enzyme is functional as a tetramer, whereasthese functions are performed by various enzymes of mammalian and yeast GS are active as dimers, whichglutathione metabolic pathway like glutathione shows that there are two families of GS. GS deficiencyreductase, glutathione peroxidase and glutathione-S- in mammals is an autosomal recessive disorder andtransferases.leads to 5-oxoprolinuria manifested by either mild ordebilitating diseases (Dahl et al., 1997), whichGlutathione is synthesized intracellularly by thesuggests that GS is essential for survival in mammals.consecutive action of γ-glutamylcysteine synthetase In P. falciparum, GSH is essential for the survival ofparasite and GSH level in infected red blood cells areCorresponding author: Prof. H. S. Banyal, Laboratory of maintained through the synthetic pathway (AtamnaParasitology and Immunology, Department of Biosciences, H.and Ginsburg, 1997). Meierjohann et al. (2002)P. University, Shimla-171 005, India.isolated gene that encodes GS in P. falciparum andE-mail: hsbanyal@yahoo.co.in
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