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Biomedical subjects

R C Mahajan

Publications and source records attributed to R C Mahajan.

At least 19 recordsLinked to original sources
PubMed1992

Plasmodium falciparum induced perturbations of the erythrocyte antioxidant system.

Erythrocyte antioxidants catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase were studied in cells harbouring different growth stages of Plasmodium falciparum. Catalase and superoxide dismutase showed significant decrease during parasite maturation indicating hampered metabolism of hydrogen peroxide and superoxide anions. Glutathione peroxidase also exhibited a downward trend during the growth of P. falciparum, while there was a moderate accumulation of reduced glutathione. These findings suggest decreased utilization of the reduction potential in detoxification of reactive oxygen species. The fall in all three antioxidant enzymes studied was highly significant (P less than 0.001) in erythrocytes with mature stages of the parasite (trophozoites, schizonts). The increased vulnerability of erythrocytes to damage, which parallels the growth phases of the parasite emphasizes the need for early treatment of P. falciparum malaria to minimise red cell destruction and the resulting anaemia.

Animals↗
PubMed1992

Study on the mechanism of Giardia lamblia induced diarrhoea in mice.

The transmucosal fluxes of Na+ and Cl- were studied in Giardia lamblia infected mice in the presence or absence of phorbol-12-myristate-13-acetate (PMA), the activator of protein kinase C (PKC) or 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7), the inhibitor of PKC or Ca(2+)-calmodulin. There was net secretion of Na+ and Cl- in infected animals, while in control animals there was net absorption of these ions. The addition of ionophore or PMA resulted in net secretion of Na+ and Cl- in the control group while in the infected group there was no change in the fluxes of these ions. The selective potent inhibitor of protein kinase C, H-7, reversed the secretion of Na+ and Cl- in infected group to absorption. The addition of PMA and Ca(2+)-ionophore together in the infected group had a partial additive effect. This study suggests that G. lamblia induced fluid secretion involves protein kinase C and further protein kinase C acts in synergism with calcium.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Oxidative damage of erythrocytes infected with Plasmodium falciparum. An in vitro study.

The extent of reduced glutathione, activity of glutathione peroxidase, amount of membrane lipid peroxidation products, and the extent of hemoglobin release from host erythrocytes during in vitro Plasmodium falciparum growth was studied. Highly synchronized parasite cultures were studied to examine the alterations caused by different growth stages of the parasite. There was a moderate increase in the reduced glutathione content as the parasite matured, which was significant only in schizont-rich erythrocyte lysates (p < 0.05) whereas the activity of glutathione peroxidase was significantly low in all the parasitized red blood cells (ring-infected RBC, p < 0.005; trophozoite- and schizont-infected RBC, p < 0.001). The lipid peroxidation product, malonyldialdehyde, of the host red cells increased gradually to more than fourfold in schizont-rich cells as compared with normal erythrocytes (p < 0.001). The hemoglobin release from cultured cells was significantly higher in all parasitized red cell cultures as well as in uninfected cells kept in in vitro, as compared with normal erythrocytes. The consequence of such changes induced by the malarial parasites in the host red cells in the pathogenesis of erythrocyte destruction and anemia of P. falciparum malaria is discussed.

Erythrocytes↗
PubMed1992

Effect of nifedipine treatment on oxidative metabolism of peritoneal macrophages and neutrophils of Plasmodium berghei-infected mice.

The oxidative metabolism of peritoneal macrophages (PM) and neutrophils from nifedipine (calcium channel blocker)-treated, Plasmodium berghei (NK 65)-infected and normal infected Swiss Albino mice was studied. A significant fall in oxidative metabolism as evidenced by decreased chemiluminescence (CL) response (P less than 0.001) was recorded both in PM and neutrophils from nifedipine-treated mice compared to the control animals. When the oxidative metabolism of these phagocytes was studied after infection of the host, higher CL response was recorded from both PM and neutrophils isolated during the early course of infection (0-1 and 5-10% parasitaemia) when compared to uninfected mice (P less than 0.001). A similar pattern was observed in the case of nifedipine-treated and infected mice even though the CL response was much lower. The increasing parasite load not only resulted in subnormal CL response but also prolonged the time required for the phagocytes to exhibit peak oxidative activity both in normal infected and CCB-treated infected mice, but the time taken to show peak CL response was shortened following drug administration compared to controls. These observations revealed the profound in vivo effect of CCB on the functioning of phagocytic leucocytes and thereby questions the use of CCB in combination with chloroquine for reversal of drug resistance.

Animals↗
PubMed1992

An experimental model of ameboma in guinea pig.

Among the wide variety of clinicopathological manifestations of intestinal amebiasis, amebomas occur rarely and their pathogenesis is not well understood. When cholesterol-fed, 2- to 4-week-old guinea pigs were infected intracecally with a virulent, monoaxenic strain of Entamoeba histolytica, gross and histologically characteristic amebomas developed in 85% of the animals by the 3rd day, in 94% by the 9th day, and in 96% by the 12th day postinfection, by which time most of them had died. Amebomas were confirmed by histopathology. Thus, a model of consistent production of amebomas was documented.

Animals↗
PubMed1992

Effect of sodium stibogluconate and pentamidine on in vitro multiplication of Leishmania donovani in peritoneal macrophages from infected and drug-treated BALB/c mice.

The in vitro antileishmanial activity of sodium stibogluconate (SSG) and pentamidine in peritoneal macrophages from three different groups of animals (i.e. normal, Leishmania donovani-infected and drug-treated BALB/c mice) is reported. Peritoneal macrophages were extracted from all these animals and infected in vitro with L. donovani promastigotes. After 24 h, the infected macrophages (with amastigotes) were exposed to various concentrations of SSG (10-90 micrograms/mL) and pentamidine (0.1-5.0 micrograms/mL). The in vitro infection could be cured readily with 80 micrograms/mL of SSG and 4 micrograms/mL of pentamidine in macrophages from normal animals. But even higher dosages of these drugs added in vitro could not reduce the amastigote loads in macrophages from infected animals. In contrast, incubation in vitro of infected macrophages with very low dosages of these drugs (40 micrograms/mL of SSG and 1.0 mu/mL of pentamidine) could eliminate the parasites present within macrophages obtained from drug-treated animals. This was probably because the macrophages from drug-treated animals tackled the parasites themselves by their microbicidal mechanisms and the in vitro infection was tackled by the drug in vitro. This implies that a well-developed specific immunity in leishmaniasis helps in the antileishmanial activity of these drugs.

Animals↗
PubMed1992

Response of mast cells against filarial antigens from experimentally infected Mastomys natelensis with Brugia malayi.

The role of antigens of Brugia malayi adult worms in induction of histamine release from mast cells was studied. Both peritoneal and lung mast cells were passively sensitized using immune serum collected from Mastomys natelensis on different days after infection with B. malayi. A significant release of histamine both with crude worm and 60-kD antigens was shown. However, the role of the 43-kD antigen in histamine release was comparable to that of control. When the sera were heat inactivated, the histamine release was minimal, thus indicating the heat-labile nature of the antibodies. Furthermore, the responses of peritoneal and lung mast cells to filarial antigens were similar.

Animals↗
PubMed1992

Inhibition of adhesion by monoclonal antibody to 66 kDa surface antigen of Entamoeba histolytica.

The adherence of E. histolytica trophozoites to target cells was studied using a monoclonal antibody to a major surface antigen of 66 kDa. Preincubation of trophozoites with monoclonal antibody decreased their ability to adhere to and engulf erythrocytes and destruction of CHO cells. The monoclonal antibody was specific for the 66 kDa antigen which is possibly a major participant in adhesion which precedes other events in phagocytosis and cytopathic effects.

Animals↗
PubMed1992

Evaluation of enzyme linked immunosorbent--assay for the detection of anticysticercus antibodies in cerebrospinal fluid from patients with neurocysticercosis.

Enzyme linked Immunosorbent Assay (ELISA) was done for the detection of antibodies to Cysticercus cellulosae in 135 cerebrospinal fluid (CSF) and 152 serum samples from patients suspected clinically of neurocysticercosis (NC), neurological disorders other than NC and controls by the use of crude cyst extract antigen. This assay was compared with the standard technique of indirect haemagglutination test (IHA). The results of the two techniques were matched with retrospective analysis of proven diagnosis of these patients. ELISA and IHA was found to be positive respectively in 88 and 84 percent of CSF and 92 and 87.2 percent of serum samples from proven NC patients. The IHA technique was found to be absolutely specific for the detection of antibodies in CSF samples while cross reactions were observed with ELISA technique in CSF from 5 patients, one each suffering from disappearing CT scan lesion, tubercular meningitis (culture negative), chronic meningitis, benign intracranial hypertension and non compressive myelopathy. However possibility of neurocysticercosis cannot be absolutely ruled out in such patients. Both the techniques were found to be highly non specific for the detection of antibodies in serum samples. The study suggests that either of the two techniques may be used for the detection of antibodies in CSF samples from clinically suspected NC patients with high degree of sensitivity and specificity.

Antibodies, Helminth↗
PubMed1991

Anti-trichomonad IgA antibodies in trichomoniasis before and after treatment.

Anti-trichomonad IgA antibodies were estimated by enzyme-linked immunosorbent assay (ELISA) in serum and vaginal secretions of 25 symptomatic and 25 asymptomatic Trichomonas vaginalis positive patients before and after treatment and in 25 age-matched controls. Significantly higher levels of antitrichomonad IgA antibodies were found in T. vaginalis positive patients when compared to control subjects, especially in vaginal secretions. In addition, a significant decrease in these antibodies was observed after treatment, which was more pronounced in vaginal secretions. It seems that anti-trichomonad IgA antibodies in serum and more so in vaginal secretions are directly related to and specific to the presence of T. vaginalis in the urogenital tract.

Adult↗
PubMed1991

In vitro effect of larval stages of Ascaris lumbricoides on human blood clotting.

The effects of larval stages of Ascaris lumbricoides on human blood clotting was studied in vitro. Extracts and excretory/secretory products of third-stage larvae (L3) and late third-stage larvae (LL3) cultured from ova obtained from infected patients were analysed for anti-coagulant activity. Prothrombin time (PT) was prolonged by the addition of either whole extract of L3/LL3 or ES products of L3/LL3 as compared to controls. Partial thromboplastin time with kaolin (PTTK) was also prolonged on the addition of either extracts of ES products of L3/LL3. The prolongation of PTTK was significantly higher with extracts/ES products of L3 when compared to the extracts/ES products of LL3 (p less than 0.005). Thrombin time (TT) was prolonged by extracts of L3/LL3 and their ES products.

Animals↗
PubMed1991

Effect of nifedipine on Leishmania donovani infection in-vivo and in-vitro: chemiluminescence responses of peritoneal macrophages and neutrophils.

After peritoneal macrophages had been exposed to different concentrations of nifedipine (10-120 ng mL-1) there was a significant increase (P less than 0.001) in the percentage of Leishmania donovani infected macrophages compared with controls. Parasite load was also significantly increased (P less than 0.001) in nifedipine-treated, L. donovani infected, BALB/c mice, compared with untreated, infected mice, post-inoculation. Peak chemiluminescence responses were significantly depressed (P less than 0.001) in nifedipine-treated infected mice compared with untreated mice post-inoculation. It is suggested that availability of intracellular calcium is a factor in the defense mechanism of inflammatory cells in L. donovani infections.

Animals↗
PubMed1991

Evaluation of RNA rich fraction of Litmosoides carinii in induction of protection in infected rats.

The RNA rich fraction of adult L. carinii worms was evaluated in evoking a protective response in infected rats. The RNA immunization was seen to be effective in limiting the microfilaraemia in peripheral blood as well as the adult worm burden. The antibodies to both RNA antigen and adult worm antigen were high in this group of animals at the peak of infection. The RNA immunization was seen to evoke hyperresponsiveness in lymphocytes to mitogens like adult worm antigen, PHA and Con A.

Animals↗
PubMed1991

Malaria screening to prevent transmission by transfusion: an evaluation of techniques.

Transfusion-associated malaria is often severe or even fatal, because diagnosis is frequently delayed and it complicates an already serious underlying disorder. Detection of infected donors is difficult in endemic areas due to the lack of a suitable donor screening test. Blood smear staining techniques show poor results due to the low parasite concentration in many infected persons, and the antibody detection test is not helpful due to the universal presence of antibody in healthy donors in these areas. For comparative evaluation of various screening tests, 9131 blood smears from voluntary donors and a group of patients were screened by Giemsa staining. Ten (0.10%) subjects showed parasitaemia, whereas Acridine Orange fluorescence staining showed 13 (0.14%) parasitaemia in almost the same number of smears screened on the same samples. Significantly high levels of malarial antibody were detected in 12.6% and 19.86% of subjects by indirect fluorescent antibody and enzyme-linked immunoassay tests, respectively. Malarial antigen detection by monoclonal antibody showed positive results in 9.48% of subjects, demonstrating excellent results and showing direct evidence of infection. We recommend that this should be adopted as a screening technique by transfusion services in endemic areas in order to prevent post transfusion malaria.

Acridine Orange↗
PubMed1991

Phagocytic capacity of Kupffer cells during hepatic amoebiasis in guinea pigs.

Very few studies have been carried out on the role of liver macrophages (Kupffer cells) during the course of hepatic amoebiasis. The kinetics of phagocytic activity of Kupffer cells and blood monocytes was studied in guinea pigs intra-mesenterically infested with Entamoeba histolytica. The phagocytic capacity of blood monocytes of normal animals was comparatively lower than Kupffer cells for both latex and haemolysin coated sheep red blood cells. Significant decline in phagocytic response of Kupffer cells and blood monocytes of infected animals was observed right from 2nd post infection day and it kept on decreasing with the progress of infection. Depression in phagocytic response of Kupffer cells and blood monocytes was more marked in those animals who had higher grades of pathological lesions. Hence, an inverse correlation was obtained between the phagocytic capacity and severity of amoebic lesions (P less than 0.01). The significance of depression in phagocytic response of Kupffer cells and blood monocytes may be responsible for the development of hepatic lesions.

Animals↗