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Biomedical subjects

P K Ray

Publications and source records attributed to P K Ray.

At least 55 records · Page 3Linked to original sources
PubMed1992

Mechanism of enhanced phagocytic response in protein a treated rat macrophages.

Protein A of S. aureus Cowan I has been shown to stimulate macrophage mediated phagocytosis. The present study was undertaken to understand the mechanism involved in the enhancement of phagocytosis of peritoneal macrophages by protein A. The lucigenin and luminol-dependent chemiluminescence (CL) of rat peritoneal macrophages, after incubation with various concentrations of protein A, flow-cytometric studies using DCFH-DA as a fluorescent compound and phagocytosis of sheep red blood cells (SRBCs) by rat peritoneal macrophages were studied. A significant increase in lucigenin dependent CL due to formation of superoxide anions (O2-.) and in luminol dependent CL due to formation of hydrogen peroxide (H2O2) was observed in protein A treated macrophages. A significant increase in intracellular hydrogen peroxide (H2O2) was also observed along with an increase in phagocytosis of SRBCs by protein A treated macrophages. The present findings indicate that protein A helps to increase phagocytosis and triggers respiratory burst of macrophages. Thus, both increased phagocytic response and respiratory burst of macrophages in protein A treated animals may be contributing to the antitumor property of protein A reported earlier.

Acridines↗
PubMed1992

Modulation of IgM to IgG class switch by protein A.

The Fc binding property of soluble protein A (SpA) from Staphylococcus aureus has been utilized to form IgG-SpA complexes which enabled an increase or decrease of IgG from the host depending on the dose of SpA administered. When 5 micrograms SpA was administered the IgG-SpA complexes were rapidly catabolized and, hence, low plasma IgG levels were observed. In contrast 25 micrograms SpA resulted in a significant increase in the IgG level in the host plasma. Based on these observations, the present investigation attempted to study the effect of IgG depletion/increase on the primary and secondary B-cell response to sheep erythrocyte (SRBC) antigen in Balb/c mice. Introduction of 5, 10 and 25 micrograms SpA at the time of the primary antigenic challenge inhibited both the primary IgM and the secondary IgM and IgG responses in a dose-dependent manner. Administration of 5 and 10 micrograms SpA at the time of the secondary antigenic challenge enabled the host to maintain the otherwise depressed secondary IgM response equivalent to the normal primary response. In contrast, 25 micrograms SpA at the time of the secondary antigenic challenge inhibited both the IgM and IgG PFC responses. These results extend our understanding of the mechanism of switch in immunoglobulin class expression during antigen driven maturation of the B-cell response.

Animals↗
PubMed1992

Induction of immune rejection of tumors by protein A in mice bearing transplantable solid tissue Dalton's lymphoma tumors.

In a transplantable solid tissue Dalton's lymphoma tumor model in mice we have studied the mode of antitumor action of protein A, a well known biological response modifier. Protein A (15 ug) was administered intravenously in normal and solid tissue Dalton's lymphoma tumor bearing mice on day 3 and 7 after tumor inoculation. Incidence of mortality was more in untreated tumor bearing group than that in PA treated tumor bearers. There was a significant decrease (p less than 0.001) in tumor diameter in PA treated group compared to untreated group. Protein A treatment significantly enhanced the delayed type hypersensitivity (p less than 0.01), T-cell number in spleens (p less than 0.001) and lymph nodes (p less than 0.05) as well as phagocytosis (p less than 0.001) of opsonized SRBC by peritoneal macrophages of tumor bearing animals. Apart from the nonspecific immunopotentiation, Protein A also activates natural Killer (NK) cell activity and also splenic lymphocytes mediated killing of autologous tumor targets in a significant (p less than 0.001) manner. These results suggest that PA treatment activates cellular arc of the immune system in general, and macrophage, T cells and NK cells specifically. In the present communication, we have attempted to provide the information that these immune activations appear to be related to antitumor response induced by Protein A.

Animals↗
PubMed1992

Effect of zinc on immune functions and host resistance against infection and tumor challenge.

The effect of zinc treatment on immune function and resistance against infection and tumor challenge was studied in mice. Swiss albino mice were treated with zinc acetate (3 mg/kg body weight) in one or two intraperitoneal injections. Various immune function assays were performed in treated animals. Zinc treatment to normal animals caused potentiation of T-lymphocyte and macrophage functions. Zinc treatment was also found to increase host resistance against Candida albicans and Semliki Forest virus infections. Increased resistance against endotoxin shock and Ehrlich's ascites tumor challenge was also observed in zinc treated animals. It can be stated from this study that zinc treatment potentiates the cell mediated immunity and host resistance against infection and tumor challenge.

Animals↗
PubMed1992

Protein A potentiates lymphokine-activated killer cell induction in normal and melanoma patient lymphocytes.

The effects of purified protein A from Staphylococcus aureus Cowan I stain on induction of lymphokine (IL-2) activated killer (LAK) activity were studied in normal as well as melanoma patient's lymphocyte. The coculture of peripheral blood mononuclear cells (PBMC) with various doses of protein A (0.001, 0.01 and 0.1 microgram/ml) and IL-2 (100 U/ml) for 4 days produced synergistic effect on the LAK cells mediated cytotoxicity. The potentiation of cytotoxicity and lytic ability of LAK cells against NK sensitive (K-562) and NK-resistant (M14) tumor cells were observed. Further there was potentiation of DNA synthesis in PBMC after 4 days culture. Similar results were found when PBMC from melanoma patients were cultured with PA and IL-2. The potentiation of LAK cell induction associated with its cytotoxic and lytic potential by low doses of IL-2/PA regiment may be helpful in the development of LAK immunotherapy of the cancer patients.

Drug Synergism↗
PubMed1991

Inhalation toxicity of methyl isocyanate: biochemical and cytological profile of bronchoalveolar lavage fluid in rats.

Acute pulmonary injury in rats following a single inhalation exposure to methyl isocyanate (3.2 mg l-1) was reflected by alterations in the biochemical and cytological constituents of bronchoalveolar lavage fluid (BALF) over a period of 30 days. Total protein, sialic acid and lactic acid contents of BALF were increased followed by a gradual decline to normalcy between day 3 and day 30 post-exposure. The activity of lactic dehydrogenase also increased progressively with time. The cellularity of BALF was increased significantly and primarily comprised of polymorphonuclear neutrophils at 8 days. The adherence of macrophages was unchanged but their viability was lowered at 30 days post-exposure. The results indicate the significance of bronchoalveolar lavage analysis in monitoring pulmonary toxicity by methyl isocyanate, which is characterized by the hypoxic condition and reduced cellular defence. Some toxic manifestations are potentially reversible with time after cessation of exposure.

Administration, Inhalation↗
PubMed1991

Effect of subchronic aflatoxin exposure on growth and progression of Ehrlich's ascites tumor in mice.

The present investigation was undertaken to assess whether aflatoxin B1 (AFB1) has any modulatory effect on the growth and progression of Ehrlich's ascites tumor (EAT) in mice or not. Male Swiss albino mice were treated with 0, 70, 350 and 700 micrograms AFB1/kg body weight in 0.2 ml corn oil on alternate days, orally, for two weeks. Treated animals were challenged with 1 x 10(6) cells of Ehrlich's ascites tumor. Animals were monitored for the appearance of palpable tumor, body weight gain as a measure of tumor burden, mortality profile and tumor cell population. Some parameters of cell mediated immunity (CMI), humoral immunity and non-specific immunity were also studied in aflatoxin treated animals in order to find out the mechanism of action of AFB1 on host immunity. It was observed that AFB1 treatment resulted in an early appearance of tumor, enhanced mortality, appreciable increase in body weight gain and EAT cell population following tumor challenge, in comparison with the control animals. Aflatoxin treatment caused suppression of CMI including an impairment of macrophage function, while humoral immunity was not much affected. It may be concluded that impaired CMI and macrophage function might be contributing to the increased growth of EAT in the AFB1 treated animals. Our findings may be relevant in that when a host is exposed to aflatoxins concomitantly with other carcinogens and cancer causing situations.

Aflatoxin B1↗
PubMed1991

A study on the B cell activity in protein deficient rats exposed to methyl isocyanate vapour.

The effect of MIC on the humoral immunity of the malnourished (protein deficient) subjects has been investigated. A single exposure of MIC (1.60 mg/l) on protein deficient rats showed no significant change in the body weight and mortality rate compared with the normal but the serum protein levels were found significantly low (P less than 0.01) in the protein deficient diet fed control (PDC) ones. Both PDC and protein deficient MIC exposed (PDMIC) rat showed diminished B-cell proliferation with the optimal dose of LPS, compared to the NDC and normal diet fed MIC exposed (NDMIC) group. Furthermore significant suppression (P less than 0.01) in the B-cell activation by LPS was observed in the PDMIC compared to PDC. The total IgM level in PDMIC was 43% less while 26% higher in NDMIC compared to NDC. The total IgG level in PDMIC and NDMIC was higher (20%) compared to NDC, while 25% less in PDC. The antigen specific B-cell immunity was affected in PDMIC, PDC and NDMIC. As the terminal differentiation process of B-cells were found equally affected in both PDC and NDMIC, it appears that MIC has no synergistic effect on the humoral immunity of the protein malnourished host.

Animals↗
PubMed1991

In vitro anti-oxidant property of protein-A of Staphylococcus aureus.

Protein-A (PA) is a cell-surface glycoprotein of S. aureus Cowan I with immunomodulatory and anti-tumor activities, and ability to ameliorate cyclophosphamide and carbontetrachloride (CCl4) induced toxicity in rodents. The likely mechanism of this effect appears to be the anti-oxidant property of PA, evidenced in the present study by inhibition of CCl4 and Fe2-ascorbate induced lipid peroxidation in rat liver homogenates and inhibition of deaminative-oxidative degradation of L-glutamate into 2-thiobarbituric acid reactive products in a constituted chemical system. The anti-oxidant property of PA seem to arise from its molecular characteristics and the ability to interact with a superoxide derived free-radical species without any affinity for superoxide anion, hydroxyl radical and singlet oxygen species.

Animals↗
PubMed1990

Induction of glutathione-S-transferase isoenzymes by protein A in rat liver.

The administration of Protein A, a cell wall protein of Staphylococcus aureus Cowan I cells, causes an induction of glutathione-s-transferase in rat liver. Proteins, cross reactive with anti human glutathione-s-transferase, acidic (pi), basic (alpha, and neutral (mu) isoenzymes, are induced by 5.8, 2.2 and 6.15 fold respectively. The induction of glutathione -s-transferases, at least in part, might play a role in manifestation of therapeutic properties of Protein A.

Animals↗
PubMed1990

Effects of aflatoxin on lymphoid cells of weanling rat.

Aflatoxin (AF), the hepatocarcinogenic food contaminant produced by the Aspergillus flavus group of fungi, is known to interact with various vital processes, including the immune function. Effects of long-term treatment of three dose levels of aflatoxin B1 (AFB1) on lymphoid cells of weanling rats were studied. AFB1 treatment caused a reduction in body weight gain, significantly (P less than 0.01) at the 700 microgram level. There was also a significant decrease in the weight of spleen and thymus in AFB1-treated animals in comparison to control. Similarly, AFB1 depleted cell populations of thymus and bone marrow and WBC and RBC counts. There was a marked reduction in the population and phagocytic capacity of macrophages due to AFB1 administration at dose levels of 350 and 700 micrograms kg-1 body weight. Macromolecular synthesis of DNA, RNA and protein in macrophages was affected, as there was significant inhibition in the incorporation of [3H]-thymidine, [3H]-uridine and [3H]-leucine. The hampered functioning of macrophages may be due to the cytotoxic action of AFB1.

Aflatoxin B1↗
PubMed1990

Effect of methyl isocyanate (MIC) on rat erythrocytes.

Changes in surface morphology of rat erythrocytes were studied by scanning electron microscopy after a single and repeated exposure of methyl isocyanate under static conditions. Marked morphological changes (echinocytes and spherocytes) were observed, followed by an increase in osmotic fragility of the erythrocyte membrane. The activity of the membrane bound enzyme adenosine triphosphatase (Na+, K+, Mg++) was inhibited.

Adenosine Triphosphatases↗
PubMed1990

Evaluation of the mutagenic potential of endosulfan using the Salmonella/mammalian microsome assay.

The mutagenic potential of endosulfan, a polychlorinated insecticide, was assessed using the highly sensitive Salmonella tester strains TA97(a), TA98, TA100 and TA102. It exhibited a toxic effect at dose levels of 50 micrograms/plate and higher. Plate incorporation studies did not show mutagenic response with any of the tester strains used. A modification of the assay using a preincubation procedure showed mutagenic activity with and without metabolic activation with TA97(a) only. Increased toxicity was observed after addition of phenobarbital-induced S9 mix.

Animals↗