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Biomedical subjects

M Chatterjee

Publications and source records attributed to M Chatterjee.

At least 37 records · Page 2Linked to original sources
PubMed2001

Cell line dependent involvement of ceramide in ultraviolet light-induced apoptosis.

Ultraviolet light (UV) activates an acid sphingomyelinase (ASMase) pathway, which hydrolyzes sphingomyeline to ceramide. Ceramide has been found to be a second messenger, which activates the c-jun N-terminal kinase (JNK) that is required for apoptotic cell death. However, the role of ceramide in UV-induced JNK activation and apoptosis remains controversial. In this study, we examined the correlation among ceramide production, JNK activation and cell apoptosis after UV-irradiation in three cell lines: 293 (kidney), Jurkat (lymphocytes) and MCF-7 (breast) were used in this study. The ceramide production was analyzed using the diacylglycerol kinase assay method. The JNK activation was measured by Western blot analysis using an antibody specifically recognizing phosphorylated JNK. Cell apoptosis was determined by morphological change or flow cytometry. Our data show that UV-irradiation induces ceramide production in both 293 and Jurkat cells. Inhibition of ceramide production by desipramine (25-50 microM) reduced UV-induced JNK activation in both 293 and Jurkat cells; and protects 293 cells from UV-induced apoptosis. However, inhibition of ceramide production does not prevent Jurkat cells from UV-induced apoptosis. In addition, our data demonstrates that UV-irradiation induces JNK activation and apoptosis of MCF-7 cells without production of detectable amounts of ceramide after UV-irradiation. These results suggest that UV-induced JNK activation and apoptosis can be mediated through a ceramide dependent or an independent pathway.

Apoptosis↗
PubMed2001

O-acetyl sialic acid specific IgM in childhood acute lymphoblastic leukaemia.

Initial studies have revealed an enhanced surface expression of O-acetylated sialoglycoconjugates (O-AcSGs) on lymphoblasts concomitant with high titres of IgG in childhood Acute Lymphoblastic Leukaemia (ALL) (Mandal C, Chatterjee M, Sinha D, Br J Haematol 110, 801-12, 2000). In our efforts to identify disease specific markers for ALL, we have affinity-purified IgM directed against O-AcSGs that reacts with three disease specific O-AcSGs present on membrane proteins derived from peripheral blood mononuclear cells (PBMC) of ALL patients. Antibody specificity towards O-AcSGs was confirmed by selective binding to erythrocytes bearing surface O-AcSGs, decreased binding with de-O-acetylated BSM and following pretreatment with O-acetyl esterase. Competitive inhibition ELISA demonstrated a higher avidity of IgM for O-AcSG than IgG. Flow cytometry demonstrated the diagnostic potential of purified O-AcSA IgM as binding was specific with ALL patients and minimal with other haematological disorders and normal individuals. It therefore may be adopted as a non-invasive approach for detection of childhood ALL. Taken together, the data indicates that carbohydrate epitopes having terminal O-AcSA alpha2 --> 6 GalNAc determinants induce disease specific IgG and IgM, potentially useful molecular markers for childhood ALL.

Antibody-Dependent Cell Cytotoxicity↗
PubMed2001

Effect of selenomethionine on N-methylnitronitrosoguanidine-induced colonic aberrant crypt foci in rats.

An association between low selenium intake and the incidence or prevalence of cancers is well known. Selenium in the form of selenomethionine supplemented in drinking water has been found to be highly effective in reducing tumour incidence and preneoplastic foci during the development of hepatocarcinogenesis in rats in our previous studies. Here, an attempt has been made to investigate whether the dose and form of selenium found to be effective during hepatocarcinogenesis is equally effective in N-methylnitronitrosoguanidine-induced colorectal carcinogenesis in terms of antioxidant defence enzyme systems, DNA chain breaks and incidences of aberrant crypt foci. Treatment with selenomethionine either on initiation or on selection/promotion, or during the entire experiment showed that selenomethionine was most effective in regulating the cellular antioxidant defence systems, DNA chain break control and reducing aberrant crypt foci in the colorectal tissues of rats. Our results also confirm that selenium is particularly effective in limiting the action of the carcinogen during the initiation phase of this colorectal carcinogenesis, just as we found with hepatocarcinogenesis in our previous studies.

Animals↗
PubMed2000

Combined supplementation of vanadium and 1alpha,25-dihydroxyvitamin D3 inhibit placental glutathione S-transferase positive foci in rat liver carcinogenesis.

The combined effects of vanadium (V) and 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] in inhibiting diethylnitrosamine (DEN)-induced and phenobarbital (PB) promoted hepatocarcinogenesis were examined in male Sprague-Dawley rats. All the rats were subjected to 70% partial hepatectomy (PH) at week 4 and 24h later were administered either solvent trioctanoin (Group B, D, F and H) or 10 mg DEN/kg (Group A, C, E and G) by gavage. Briefly after two weeks of DEN administration, PB were administered (0.05% in basal diet) to all the DEN-treated rats and continued till the completion of the experiment. Supplementary V at the dose of 0.5 ppm in drinking water ad libitum (Group C and D), 1,25(OH)2D3 at the dose of 3 microg/ml in propylene glycol per os twice a week (Group E and F) or both V and 1,25(OH)2D3 at the same above given doses (Group G and H) were started 4 weeks prior to DEN administration (week 0) and continued thereafter till week 15. The expression of the number and area of altered hepatocyte foci (AHF) positive for placental glutathione S-transferase (GST-P) was maximum in DEN-treated and PB promoted group (Group A). V (Group C) and 1,25(OH)2D3 (Group E) treatment significantly reduced the expression of GST-P-positive hepatocytes by 36.02% and 45.16% respectively but an additive protective action (61.46%) was found in Group G which received both V and 1,25(OH)2D3 for the entire period of the study. Moreover, histopathological examination and the incidence of hepatic hyperplastic nodules showed that combined action of V and 1,25(OH)2D3 can able to minimize the appearance of nodules as well and maintain the normal cellular architecture than V and 1,25(OH)2D3 when given alone. These results suggest that, when given together V and 1,25(OH)2D3 could be the chemopreventive agents for rat liver carcinogenesis.

Administration, Oral↗
PubMed2000

Inhibition of diethylnitrosamine-induced rat liver chromosomal aberrations and DNA-strand breaks by synergistic supplementation of vanadium and 1alpha,25-dihydroxyvitamin D(3).

Vanadium (V) has recently been found to possess potent anti-neoplastic activity in rat hepatocarcinogenesis. Recent studies have suggested that the active metabolite of vitamin D(3), 1alpha, 25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], can inhibit growth and/or induce differentiation of a variety of cell types. In the present study, attempts have been made to investigate the combination effects on chromosomal aberrations (CAs) and DNA-strand breaks during the early preneoplastic stage of diethylnitrosamine (DEN)-induced rat liver carcinogenesis in male Sprague-Dawley rats. V (0.5 ppm ad libitum) and/or 1,25(OH)(2)D(3) (0.3 microg/0.1 ml propylene glycol per os twice weekly) either alone or in combination were given to DEN-treated and control rats 4 weeks prior to DEN injection. Under these experimental conditions it was observed that, when given in combination, V and 1,25(OH)(2)D(3) offered maximum protection against DEN-induced structural aberrations 96 h (66.7%, P<0.05), 15 days (44.9%, P<0.005) and 30 days (63.8%, P<0.001) after DEN injection. Synergistic supplementation of both V and 1, 25(OH)(2)D(3) 4 weeks before DEN injection was found to offer significant (64.1%, P<0.001) protection against generation of single-strand breaks when compared with the DEN control. Thus, the combination effect of V, an essential trace element, and of 1, 25(OH)(2)D(3), a dietary micronutrient, appears beneficial in preventing genetic damage in liver cells upon alkylation induced by DEN.

Animals↗
PubMed2000

Combined supplementation of vanadium and 1alpha,25-dihydroxyvitamin D(3) inhibit diethylnitrosamine-induced rat liver carcinogenesis.

A combination of a differentiation-inducing agent like 1alpha, 25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] with a compound that blocks entry of calcium into cells like vanadium (V) may offer a new approach to differentiation therapy and address the problem of hypercalcemia. Initiation of hepatocarcinogenesis was performed by a single intraperitoneal injection of diethylnitrosamine (DEN) (200 mg/kg b.wt.) in male Sprague-Dawley rats. Supplementation of V, 1, 25(OH)(2)D(3), or both V and 1,25(OH)(2)D(3) were started 4 weeks prior to DEN injection and continued thereafter till 20th week. It was observed that supplementation of V (0.5 ppm) in drinking water ad libitum or 1,25(OH)(2)D(3) (3 microg/ml propylene glycol) per os twice weekly for the entire period of the experiment significantly reduces the number and size of hyperplastic nodules while the combination treatment offered an additive effect in reducing it to 37.5% from 83.3%. V-1,25(OH)(2)D(3) combination was also effective in elevating the level of hepatic microsomal cytochrome P-450 (Cyt. P-450) (P<0.001). Moreover, A significant reduced level of cytosolic glutathione (GSH) (P<0.001) and glutathione S-transferase (GST) (P<0.001) activity as well as reduction in the appearance of gamma-glutamyltranspeptidase (GGT)-positive foci (P<0.001) as compared to carcinogen control were observed in V plus 1, 25(OH)(2)D(3) treated group. These results suggest that V may be useful in combination with 1,25(OH)(2)D(3) in the inhibition of experimental rat hepatocarcinogenesis.

Animals↗
PubMed2000

Anticlastogenic potential of 1alpha,25-dihydroxyvitamin D3 in murine lymphoma.

Vitamin D3, having gained scientific interest for so long because of its role in mineral homeostasis, has now received great importance as a possible antitumor agent. This study was undertaken in an attempt to visualize the possible anticlastogenic potential of the vitamin in an ascitic mouse lymphoma model namely, Dalton's lymphoma. Frequencies of structural type chromosomal aberrations, sister chromatid exchanges and micronucleus assays have been chosen as the genotoxic endpoints in the proposed investigation. All these cytogenetic markers have been found to be markedly elevated during the progression of lymphoma in bone marrow cells. Vitamin D3 effectively suppressed the frequencies of chromosomal aberrations and sister chromatid exchanges in the lymphoma-bearing mice during the entire phase of tumor growth that significantly coupled with almost two-fold increase in survival time (37 +/- 2 and 68 +/- 2 days in lymphoma controls and vitamin D3-treated lymphoma-bearing mice, respectively), thus substantiating the antineoplastic efficacy of this secosteroid. The outcome of this study also is clearly reflected in the depletion of circulating (serum) vitamin D3 levels in the lymphoma control mice compared with normal (vehicle) controls while a still higher level was maintained in the VD3-treated lymphoma mice. This anticlastogenic property of the vitamin has so far been neglected and this is the first attempt to unravel the vitamin D3's effect in combating tumor development in vivo by limiting the frequencies of chromosomal aberrations, sister chromatid exchanges and micronuclei at least in transplantable murine model studied herein.

Animals↗
PubMed2000

Beta-carotene prolongs survival, decreases lipid peroxidation and enhances glutathione status in transplantable murine lymphoma.

Carotenoids of dietary origin have recently been the subject of renewed research interest because of epidemiological evidence indicating an inverse relationship between intake of carotenoids-rich plant substances and risk of certain cancers. This study was attempted to understand the biological actions of dietary beta-carotene (BC) on Dalton's lymphoma (DL), a rapidly proliferating transplantable tumor, in effecting the survival of the lymphoma-bearing mice. The glutathione (GSH) level and the extent of lipid peroxidation in the liver, kidney and brain were monitored in BC-treated (100 mg/kg food) mice transplanted with DL. These markers showed substantial alterations during the whole length of tumor progression in lymphoma-bearing mice without BC supplementation. When treated with BC, both malondialdehyde contents (evidence of lipid peroxidation) and the GSH levels in different organs were found to be closer to normal values in the initial period of tumor progression. BC-mediated protection against lipid peroxidation was maximally found to be in hepatic tissue throughout the study following DL transplantation. This was fairly reflected in the higher BC concentration in hepatic tissue of BC-treated lymphoma group compared to untreated lymphoma control. Significantly higher survival time (51-55 days) was observed in BC-treated animals in comparison to their untreated DL counterparts (35-38 days). The prolonged survival observed in the BC-supplemented animals may be attributed to the higher resistance offered by animals receiving BC towards lipid peroxidation-related tissue injury.

Animals↗
PubMed2000

Vanadium chemoprevention of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinogenesis: probable involvement of representative hepatic phase I and II xenobiotic metabolizing enzymes.

Vanadium, a non-platinum group metal and dietary micronutrient, is now proving to act as a promising antitumor agent. The present study was conducted to ascertain its antineoplastic potential against an experimental mammary carcinogenesis. Female Sprague-Dawley rats, at 50 days of age, were treated with 7,12-dimethylbenz(a)anthracene (DMBA) (0.5 mg/100 g body weight) by a single tail vein injection in an oil emulsion. Vanadium (ammonium monovanadate) at the concentration of 0.5 ppm was supplemented in drinking water and given ad libitum to the experimental group immediately after the carcinogen treatment and it continued until the termination of the study (24 weeks for histological and biochemical observations and 35 weeks for morphological findings). It was found that vanadium treatment brought about a substantial protection against DMBA-induced mammary carcinogenesis. This was evident from histological findings that showed no sign of hyperplasia or abnormality after vanadium treatment. There was a significant reduction in incidence (P < 0.05), total number, multiplicity (P < 0.01) and size of palpable mammary tumors and delay in mean latency period of tumor appearance (P < 0.001) following vanadium supplementation compared to DMBA control. From the cumulative results of various hepatic biochemical indices namely, lipid peroxidation, reduced glutathione level, superoxide dismutase activity, cytochrome P450 content and glutathione S-transferase activity, the anticarcinogenic potential of vanadium was well reflected through stabilization of these parameters. Results of the study indicate that the anticarcinogenic activity of vanadium during DMBA-initiated mammary carcinogenesis is mediated through alteration of hepatic antioxidant status as well as modulation of phase I and II drug metabolizing enzymes. On the basis of the observed results, vanadium can be considered as a readily available, promising and novel cancer chemopreventive agent.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2000

Antioxidant associated chemoprevention by selenomethionine in murine tumor model.

Effectiveness of selenium in different forms like sodium selenite, selenocysteine and selenomethionine has been compared in four different doses, namely 4, 6, 8 and 10 ppm of each, in terms of their bioavailability and prolongation of survival of Dalton's lymphoma (DL) bearing mice. Selenomethionine, at a dose of 8 ppm, was found to be the most bioavailable and least-cytotoxic form that was capable of increasing the life span of the tumour bearing hosts maximally (almost two-fold). Beneficiality of selenomethionine has also been studied by observing continuous changes brought about by this compound on the glutathione (GSH) level, glutathione peroxidase (GPx) activity and extent of lipid peroxidation in the hepatic tissue of the tumour bearing hosts, which are indispensable for a cell to function normally and are found to exhibit significantly altered behaviour in neoplastic cells. Selenomethionine caused the maintenance of high steady state GSH level and a normal GPx activity during the fist phase of tumour growth. It also controlled lipid peroxidation during the first 15-20 days following tumour transplantation. These conditions helped in the maintenance of intracellular redox balance, cellular integrity and metabolic rhythms of cells in DL bearing mice receiving selenomethionine.

Animals↗
PubMed2000

Biochemical, haematological and histopathological study in relation to time-related cadmium-induced hepatotoxicity in mice.

In the present investigation sub-chronic hepatic necrosis was induced by cadmium chloride and was examined biochemically, haematologically and histopathologically in order to study the time-dependent effect and correlation among the parameters. Male Balb/c mice were injected with cadmium chloride (2.5 mg/kg bw s.c.) for each other day and, sacrificed on the 7th day, 14th day and 21th day post exposure. Body weight and relative liver weight did not show alteration at any of the time point following the treatment but the tissue cadmium level showed progressive significant increment values with the advancement of time exposure. Most of the biochemical parameters (total protein, DNA, RNA, cytochrome P450 cotents, alkaline phosphatase and UDP glucuronyl transferase activities), haematological parameters (total red blood cells, total white blood cell, differential white blood cell counts, haemoglobin, erythrocyte sedimentation rate, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, plasma protein) indicated either no or less on the alterations/7th day following cadmium exposure. Both the light and transmission electron microscopy, on the other hand, indicated the fact that a minimum of 21 day-exposure was needed to alter the cellular architecture. So, a certain amount of cadmium load might be required to adversely affect the cellular architecture preceeded by biochemical and haematological alterations. In this connection, in the present study a possible mechanism of cadmium-induced hepatoxicity was discussed.

Animals↗
PubMed2000

Role of linkage specific 9-O-acetylated sialoglycoconjugates in activation of the alternate complement pathway in mammalian erythrocytes.

Substitution of the -OH group at C-9 of sialic acid by an O-acetyl ester has been suggested to modify various biological phenomena that are regulated by sialic acids. Amongst them, enhancement of erythrocyte lysis by 9-O-acetylated sialic acid determinants through modulation of the alternate pathway of complement has been extensively studied on murine erythrocytes [1]. A variable expression of linkage specific 9-O-acetylated sialoglycoconjugates as defined by the lectinogenic epitope of Achatinin-H namely 9-O-acetylated sialic acid alpha2-->6Gal NAc was identified on rabbit, guinea pig, hamster, rat, mouse and human erythrocytes. This differential expression of linkage specific 9-O-acetylated sialoglycoconjugates strongly correlated with the susceptibility of mammalian erythrocytes to lysis by the alternate pathway of complement. Additionally, low levels of antibodies directed against O-acetylated sialic acids in these mammalian species suggested that these constitutively present determinants have low immunogenicity. Taken together, our results indicate that complement mediated hemolysis depends not simply upon the extent of surface 9-O-acetylated sialic acids present but more importantly upon the specific linkage.

Acetylation↗
PubMed2000

Identification and purification of cytolytic antibodies directed against O-acetylated sialic acid in childhood acute lymphoblastic leukemia.

Sialic acids typically present as terminal sugars of oligo-saccharides are reported to be modified by O-acetylation at the C-9 position on lymphoblasts of childhood acute lymphoblastic leukemia (ALL) patients (Sinha et al., 1999a, Leukaemia, 13, 119-125). We now report high titers of IgG antibodies directed against O-acetylated derivatives of sialic acids (O-AcSA) in serum of ALL patients. These antibodies were purified using bovine submaxillary mucin (BSM) and the IgG distribution was confined to IgG(1)and IgG(2)subclasses; their binding was totally abolished with de-O-acetylation confirming their specificity towards O-AcSA determinants. Flow cytometry demonstrated binding of these antibody fractions to peripheral blood mononuclear cells (PBMC) of both T- and B-ALL patients having increased cell surface 9-O-AcSA determinants. Western blotting of membranes derived from PBMC of ALL patients confirmed binding of the antibody to O-acetylated sialoglycoconjugates corresponding to 144, 135, 120, 90, and 36 kDa whereas binding to PBMC from normal individuals corresponded to 144 and 36 kDa. Specificity of the antibody fraction towards 9-O-AcSA was substantiated by hemagglutination and hemagglutination-inhibition assays. The antibody purified from ALL serum selectively mediates complement dependent cytolysis of lymphoblasts expressing O-AcSAs and thereby possibly confers passive protection. The enhanced anti O-AcSA antibody levels allowed for development of a serodiagnostic assay (BSM-ELISA) specific for ALL. Minimal crossreactivity was observed with other hematological disorders like acute myeloid leukemia (n = 16), chronic myeloid leukemia (n = 6), chronic lymphocytic leukemia (n = 7) and non-Hodgkin's lymphoma (n = 3) as well as normal healthy individuals (n = 28). The BSM-ELISA therefore provides a simple, noninvasive alternative diagnostic approach for ALL and merits clinical consideration.

Acetylation↗
PubMed2000

Effects of phase duration and electrode separation on loudness growth in cochlear implant listeners.

Loudness estimates were obtained in a group of four adult subjects implanted with the Nucleus-22 multielectrode cochlear implant device, for a range of pulse amplitudes and different fixed phase durations and electrode separations. The stimulus was a 200-ms long train of biphasic pulses presented at 500 pulses/s. Subjects estimated loudness as a number from 0 ("don't hear it") to 100 ("uncomfortably loud"). Loudness was found to grow exponentially with pulse amplitude, at a rate that was dependent upon the phase duration as well as the electrode separation. An equation of the form L = e(lambda + gamma M)(D theta)I, where L is the estimated loudness, M is the separation between electrodes of a stimulating pair, D is the phase duration, I is current amplitude, and lambda, gamma, and theta are constants, appears to describe the observed data adequately. The findings are remarkably consistent across subjects.

Adult↗
PubMed2000

Further evidence for chemopreventive potential of beta-carotene against experimental carcinogenesis: diethylnitrosamine-initiated and phenobarbital-promoted hepatocarcinogenesis is prevented more effectively by beta-carotene than by retinoic acid.

The comparative effectiveness of beta-carotene (BC) and retinoic acid (RA) was investigated against two-stage rat liver carcinogenesis initiated by a single injection of diethylnitrosamine (DEN, 200 mg/kg i.p.) followed by promotion with phenobarbital (PB, 0.05%) in a basal diet. BC (500 mg/kg) or RA (200 mg/kg) was administered per os daily throughout the entire experiment, before the initiation, or during the promotional stage. Treatment with BC throughout the experiment or before initiation significantly reduced the incidence (p < 0.01), multiplicity (p < 0.05), and size of visible subcapsular hepatocyte nodules (HNs) and reduced (p < 0.001 or 0.05) nodular volume as a percentage of liver volume. The results with RA were of lesser extent than those observed with BC. There was a considerable depletion of hepatic BC and total vitamin A (retinol + ester) in HNs and nonnodular surrounding parenchyma (NNSP) of rats subjected to the DEN-PB regimen than their control counterparts. Treatment with BC significantly elevated hepatic BC and total vitamin A contents in HNs and NNSP compared with DEN-PB control, and the elevation was proportional to the duration of BC treatment. Long-term BC or RA treatment elicited a substantial decrement in reduced glutathione content and gamma-glutamyltranspeptidase activity and an increment in cytochrome P-450 content and glutathione peroxidase and glutathione S-transferase activities in the HNs and NNSP, which were otherwise reversed in rats that received DEN-PB treatment alone. Our results suggest that BC or RA has the potential to inhibit DEN-induced hepatocarcinogenesis through selective modulation of the antioxidant defense system and xenobiotic detoxification in the liver. It is also apparent that the beneficial effect of BC or RA is primarily exerted on the initiation phase and secondarily during the promotional stage of DEN-initiated rat liver carcinogenesis and that BC affords a better chemopreventive response than RA.

Alkylating Agents↗
PubMed2000

Identification of archetype and rearranged forms of BK virus in leukocytes from healthy individuals.

BK virus (BKV) establishes a persistent, asymptomatic infection in more than 80% of the human population, and in immunocompromised individuals BKV causes acute urinary tract infections. Two forms of BKV, archetype and rearranged, have been recovered previously from urine samples. The rearranged form is believed to have emerged from the archetype form by the deletion and duplication of sequences within the transcriptional control region (TCR). We have PCR-amplified unique rearranged forms of the BKV TCR from peripheral blood leukocytes (PBLs) of healthy donors. By employing archetype-specific PCR primers, the archetype BKV TCR was also detected in PBLs. These findings are consistent with the hypotheses that PBLs transport BKV to different sites within the body and play a role in the TCR rearrangement process. BKV sequences were detected in 21 of 38 BKV-seropositive and 1 of 2 BKV-seronegative individuals. Because of recent suggestions that SV40 may circulate in the human population, the donors' sera were also examined for the presence of specific anti-SV40 antibodies. A high antibody titer to SV40 was detected in only 1 of the 40 donor specimens. This study is the first to characterize multiple BKV TCR variants in PBLs from healthy people and to correlate PCR and serological methods used to detect BKV infections.

Antibodies, Viral↗
PubMed1999

Diagnostic and prognostic potential of antibodies against O-acetylated sialic acids in canine visceral leishmaniasis.

Employing bovine submaxillary mucin (BSM) as the coating agent, an enzyme-linked immunosorbent assay (BSM-ELISA) was developed to detect antibodies directed against O-acetylated sialic acids (O-AcSA) in canine visceral leishmaniasis (CVL). Serum samples were collected from 50 dogs previously screened by a parasite-ELISA to detect anti-leishmanial antibodies and designated as seropositive (n = 30) and seronegative (n = 20). The BSM-ELISA detected anti-O-AcSA antibodies in 29 out of 30 seropositive dogs and was negative in 15 out of 20 seronegative dogs; the sensitivity and specificity of the assay being 96.6% and 75%, respectively. Seven dogs from an endemic area in central Israel were longitudinally monitored for 15 months clinically, serologically and cultured for parasite. The levels of antibodies directed against O-AcSA increased with the appearance of clinical symptoms and/or seropositivity, disappeared when the disease was self-limiting as also with chemotherapeutic response and reappeared with relapse. The BSM-ELISA, therefore, represents a valuable tool for assessment of disease progression.

Acetylation↗