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Biomedical subjects

P K Ray

Publications and source records attributed to P K Ray.

At least 109 records · Page 6Linked to original sources
PubMed1987

Increased macrophage activity in protein A treated tumor regressed animals.

Male swiss albino mice transplanted with 1 x 10(6) viable fibrosarcoma tumor cells were treated with Protein A (60 micrograms/kg) right from the day of transplantation for 4 weeks, twice weekly. The therapy resulted in lesser tumor incidence, significant inhibition of tumor growth and enhanced percent survival in treated animals as compared to untreated controls. Treated animals also showed gains in body weight, an increase in peripheral blood leucocyte count, significant increase in macrophage function and number. Stimulation of macrophage number and macrophage function by Protein A may be related to its antitumor.

Animals↗
PubMed1986

Modulation of benzene toxicity by an interferon inducer (6MFA).

Repeated intraperitoneal administration of benzene (1.0 ml/kg body wt) for 3 days produced leucopenia, lymphocytopenia and an increased number of nucleated cells in the bone marrow and significantly decreased organ weights of thymus (P less than 0.001) and spleen (P less than 0.001) in female albino rats. Iron content, lipid peroxidation and superoxide dismutase activity of the liver and bone marrow were significantly increased as a result of benzene exposure. Prior administration of 6MFA, an interferon inducer with immunomodulating potential, was found to ameliorate some of the adverse effects of benzene as well as restoration of hepatic architecture histologically. Lipid peroxidation and iron content were both normalised, whereas superoxide dismutase activity was further increased and the number of lymphocytes and bone marrow cells returned to normal. Pretreatment of animals with 6MFA was able to enhance the SRBC antibody titre in benzene-treated immunosuppressed animals. The beneficial effects of 6MFA in the amelioration of the acute toxicity of benzene therefore assume certain significance.

Animals↗
PubMed1986

Endosulfan induced inhibition of 3H-5-hydroxytryptamine uptake in platelets.

Endosulfan, a chlorinated pesticide, is widely used to control various insect pests. Rats exposed to 1 mg and 3 mg endosulfan/kg for periods of 10, 30, and 60 days showed significant (P less than 0.05) inhibition of [3H]5-hydroxytryptamine (5-HT) uptake by platelet-rich plasma (PRP) in an ex vivo study. Rats treated with endosulfan (1 and 3 mg/kg) up to 60 days elucidated a marked inhibition of ADP-induced aggregatory responses of the platelets. Incubation of PRP with 10 microM and 100 microM endosulfan for 15 min at 37 degrees C also resulted in significant (P less than 0.05) inhibition of platelet aggregation in vitro. The paper discusses the use of rat blood platelets as a model for the study of neuro- and cardiovascular toxicity of endosulfan.

Animals↗
PubMed1985

Introduction of bacterial components in postadsorbed plasma during adsorption with Staphylococcus aureus.

In vitro plasma adsorption over either protein A-positive Staphylococcus aureus Cowan I (SAC) or protein A-negative S. aureus Wood 46 (SAW) led to leaching of bacterial biomolecules in the postadsorbed plasma. Presence of bacterial moieties was demonstrated in the postadsorbed plasma by more than one method: (1) using radiolabeled bacteria for adsorption with plasma and detecting radioactivity in the postadsorbed plasma, (2) gel filtration of pre- and post-adsorbed plasmas over Sephadex G-200 column and detecting additional peak(s) in the postadsorbed plasma, and (3) immunoelectrophoretic analysis of pre- and postadsorbed plasmas and their column fractions against rabbit anti-SAC antisera and demonstrating new precipitin bands in postadsorbed plasma. Using an extracorporeal plasma adsorption procedure in mongrel dogs, with radiolabeled SAC as the adsorbent, we have demonstrated the presence of radioactivity in both the adsorbed and filtered (0.2 micron) blood entering into the body, and the adsorbed blood that passed out of the body to reenter into the extracorporeal circuit. These data suggest that components of S. aureus origin enter into the host circulation during both in vitro and ex vivo plasma adsorption, although the exact nature of those extracted staphylococcal components remains unknown. This observation is of much significance since it can possibly help elucidate the mechanism of tumor regression observed following perfusion of plasma over SAC or SAW, followed by its reinfusion to the host.

Animals↗
PubMed1985

Immunosuppressor control as a modality of cancer treatment: effect of plasma adsorption with Staphylococcus aureus protein A.

In tumor-bearing hosts both cellular and humoral tumor-growth-enhancing factors are present. They cause immunosuppression and facilitate the growth of tumors. Very early during tumor growth these factors are either elicited by the tumor cells or induced by the host immunocytes. Among these immunosuppressive agents, circulating immune complexes appear to play a predominant role. They also activate suppressor cell activity. Plasma adsorption of CIC and IgG by protein A of Staphylococcus aureus has been reported to cause tumor regression. Plasma adsorption with protein A-collodion charcoal, protein A-silica, or protein A-Sepharose also induced tumorilytic reactions. Even direct infusion of protein A induced tumor regressions in rat mammary tumors. Recent studies showing tumor regressions following S. aureus Wood 46 plasma adsorption or infusion of normal plasma adsorbed over S. aureus indicate that specific blocking factor removal by plasma adsorption may not be the mechanism for causing tumor destruction. Results indicate that S. aureus plasma adsorption leaches a number of staphylococcal agents. Thus, it appears that staphylococcal agents, protein A, enterotoxin, and other factors are responsible for the induction of reactions leading to tumor destruction. A unified mechanism explaining the results obtained with plasma adsorption using protein A of S. aureus, or S. aureus Wood, or direct protein A infusion, was presented.

Animals↗
PubMed1985

In vivo protection by protein A of hepatic microsomal mixed function oxygenase system of cyclophosphamide-treated rats.

At a high dose, cyclophosphamide (Cy, 200 mg/kg) causes depression of the enzyme activity of the hepatic mixed function oxygenase (MFO) system in Sprague-Dawley rats. The present report provides evidence for the early regeneration of the depleted enzyme activity in Cy-treated rats by purified protein A (P) of Staphylococcus aureus. Enzymes of the MFO system, such as aminopyrine demethylase and aryl hydrocarbon hydroxylase, were assayed and the content of cytochrome P-450 was determined. Inoculation of P (60 micrograms/kg) prior to Cy inoculation provides a better effect than P administration after Cy. The exact mechanism of P action is unknown. P-treated animals appear to have an ability to repair the damage caused by the toxic metabolites of Cy earlier than those in the Cy group. This property of protein A may become useful in accelerated regeneration of the enzyme activity in the hepatic MFO system following the toxic insult of Cy metabolites.

Animals↗
PubMed1985

Rescue of rats from large dose cyclophosphamide toxicity using protein A.

Cyclophosphamide (Cy) is widely used as an effective cytotoxic drug, but its use is limited because of its toxicity. In this report, we describe for the first time the ability of purified protein A (P) of Staphylococcus aureus to reduce Cy-induced toxicity in rats. Protein A-treated animals recover quickly from the toxic effects of Cy. The antitumor property of Cy is not reduced in the P + Cy group. In fact, the latter showed a persistent decrease in tumor volume compared with the Cy group. Protein A may prove to be an effective agent in increasing the therapeutic index of Cy.

Agranulocytosis↗
PubMed1985

Some observations on the macula of pesticide workers.

To study the retinal changes in occupationally exposed pesticide workers, 79 subjects exposed to an organophosphate, fenthion, and 18 exposed to an organochlorine pesticide DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane], were subjected to a detailed study, including history taking, physical examination and ophthalmic evaluation. Fluorescein angiography was performed in selected cases. Serum cholinesterase level in 22 workers and serum DDT residue in 17 workers of the respective groups were also estimated. Fifteen workers (19%), who were exposed to fenthion had macular changes (P less than 0.01). The macular lesions were characterized by perifoveal irregularity of pigmentation and areas of hypopigmentation of 1/8-1/3 disc diameter. Mean age of the subjects having macular involvement was 30.6 years and mean duration of exposure 7.9 years. The symptoms reported by them were diminution of vision (8), dislike for bright light, flash of light, black dots in front of the eyes (2 each) and visual blurring (1). Paracentral scotoma and constriction of peripheral field were present in three workers each. Fluorescein angiography suggested pigment epithelium defect. Other causes of macular involvement in these workers were excluded; a possible role of pesticides in the genesis of these macular changes is suggested.

Adolescent↗
PubMed1985

Changes in the surface fine structure of ependyma of the rat third ventricle following operative leakage of cerebrospinal fluid.

The role of the ventricular ependyma in the elaboration of cerebrospinal fluid under resting conditions is well documented. In an attempt to elucidate its response to cerebrospinal fluid leakage, male young adult Wistar rats were subjected to lumbar spinal transection under intraperitoneal Nembutal anaesthesia. Control animals received a sham operation, involving opening up the cerebrospinal fluid space and its closure. A scanning electron microscopical study of the third ventricular ependyma on the seventh postoperative day revealed pronounced surface modifications in the experimental animal which included (i) bulbous dilatations in the ciliary shafts with frequent apical blebbing, and an overall turgid appearance of most cilia; (ii) a profusion of tall and stout microvilli in the non-ciliated zones; (iii) an increase in the size and number of blebs; and (iv) a greater number of supraependymal cells especially on the ventricular floor. The significance of these changes is discussed in the light of available studies. The results, considered collectively, seem to reflect an augmented activity of the ventricular ependyma as a compensatory measure to counteract the effects of cerebrospinal fluid leakage caused by surgical trauma. Such activity may be both absorptive and secretory in nature.

Animals↗
PubMed1984

Antitumor activity with nontoxic doses of protein A.

This report confirms our previous observation that IV inoculation of purified protein A causes regression of rat mammary adenocarcinomas. In treated tumors, we have obtained histological evidence of changes indicating tumor cell destruction. Protein A treatment does not cause reduction in the body weight or organ weights of rats; nor does it cause any decrease in activity of the enzymes of the microsomal mixed function oxidase system in the liver. Protein A stimulates peripheral white cell counts in normal rats, but not in tumor-bearing rats. We found that protein A infusion reduced (P less than 0.0005) the level of circulating plasma immune complex concentration. A homing study with 125I-labeled protein A indicated that liver, spleen, and kidney tissues are the major sites of protein A accumulation. Therefore, protein A seemed to exert its antitumor effects without causing any generalized toxicity to the system. It is postulated that the action of protein A may be related to its ability to cause a drastic reduction in circulating plasma immune complex concentration, thus potentiating the immune reactivity of the host observed earlier.

Adenocarcinoma↗
PubMed1984

Ligational behavior of a novel biologically active donor toward Cu(II) and Ni(II) ions and potentiation of its antibacterial activity by chelation with metal ions.

The chelating behavior of a new multidentate ligand with tuberculostatic activity toward Cu(II) and Ni(II) ions has been studied. This ligand 3-(2-carboxyhydrazine)phenylimino-2-oximobutane(H2C POB) is found to chelate the above metal ions in both its keto and enol forms. The probable structures of all the complexes and the location of the bonding sites have been established through magnetic and spectroscopic (infrared, electronic) studies. The Cu(II) complex of the enol form exhibits subnormal magnetic moment at room temperature, indicating the probable existence of some sort of super exchange phenomenon in the system. The ligand itself and a few of its Cu(II) complexes have been found to exert powerful in vitro antibacterial activity toward some tuberculosis mycobacteria, such as Mycobacterium flae, Mycobacterium smegmatis, and Mycobacterium H37Rv.

Antitubercular Agents↗
PubMed1984

Adsorption of plasma from tumor-bearing hosts over protein A--containing nonviable Staphylococcus aureus Cowan I: possible mechanism of antitumor reactions.

Adsorption of autologous plasma over nonviable Staphylococcus aureus Cowan I (SAC) followed by reinfusion of the plasma causes regression of (a) chemically induced rat mammary adenocarcinomas (MA), and (b) canine transmissible venereal tumors (TVT) and spontaneously occurring dog tumors. Animal data are more impressive than that from trials in humans. Nine of 41 patients receiving perfusions of adsorbed plasma showed some partial objective response. Eight of these nine patients received multiple perfusions over a period of time. Twenty-one of 41 patients showed subjective responses. Adsorption of autologous plasma over non-protein A--containing S. aureus Wood 46 caused regression of MA. Adsorption of normal rat plasma with SAC, and infusion of this adsorbed plasma into mammary tumor--bearing rats, caused regression of MA. Intravenous infusion of purified protein A alone caused regression of both rat MA and canine TVT. Superimposed on this observation is the finding that, during plasma adsorption, bacterial moieties leach from SAC. It is possible that the immunostimulation observed in plasma-perfused hosts is due to the removal of plasma blocking agents on one hand, and introduction of the bacterial agents on the other.

Adenocarcinoma↗
PubMed1984

Demonstration of two distinct antibodies in autoimmune hemolytic anemia with reticulocytopenia and red cell aplasia.

To determine the mechanism of the aplastic crisis in a patient with autoimmune hemolytic anemia (AIHA) and reticulocytopenia who developed red cell aplasia simultaneously, serum- and IgG-separated fractions were examined for the presence of erythroid progenitor cell inhibitors. The patient's red cell autoantibody was a complement-independent IgG that reacted with the little-e antigen of the Rh complex. A complement-dependent serum IgG inhibitor directed against erythroid colony- and burst-forming units but not granulocyte-macrophage units was detected in samples before treatment with extracorporeal staphylococcal protein-A immunoadsorption and corticosteroids. The erythroid progenitor cell inhibitor persisted in samples multiply adsorbed against type-ee red cells and was not detected in heat eluates prepared from these red cells. A reticulocytosis occurred when serum IgG levels were reduced to 27% of pretreatment values. At this point, the erythroid progenitor cell inhibitor was not detectable in vitro. These findings suggest that the development of the aplastic crisis in some patients with AIHA may be associated with the presence of two distinct IgG antibodies, one directed at the mature red cell and the other at the erythroid progenitor cells.

Aged↗
PubMed1984

Effect of frequency of plasma adsorption over protein A-containing Staphylococcus aureus on regression of rat mammary adenocarcinomas: modification of antitumor immune response and tumor histopathology.

Adsorption of the plasma of Sprague-Dawley rats having 7, 12-dimethylbenzanthracene (DMBA)-induced primary mammary adenocarcinomas with protein A-containing Staphylococcus aureus Cowan I (SAC) and reinfusion of the adsorbed plasma caused significant (p less than 0.05) regression of mammary adenocarcinomas. Adsorption of plasma was done at different intervals--weekly, biweekly, and on alternate days. Of these protocols, alternate-day adsorptions induced very fast (within a week) tumor regression (p less than 0.001). Other protocols also produced tumor regression; however, the effect was delayed. In long-term studies, the responding animals showed fewer tumor nodules than did the untreated controls. The plasma of the treated animals showed (a) a reduction in blocking activity, (b) an increase in antibody- and complement-mediated cytotoxicity, and (c) potentiation of the cytotoxic activity of peripheral blood mononuclear cells (PBMCs). Histopathological analyses of biopsied sections of tumors from treated animals showed (a) disruption of tumor cell architecture, (b) loss of glandular structure, (c) shrinkage of epithelial cells, and (d) moderate mononuclear cell infiltration. Thus, adsorption of the plasma of DMBA tumor-bearing rats with SAC allows an indigenous immune mechanism to function against autochthonous tumors to control their growth and cause regression.

Adenocarcinoma↗
PubMed1984

Response of ependyma of the rat third ventricle to operative loss of cerebrospinal fluid: a transmission electron microscopical study.

The ependyma of the cerebral ventricles has been implicated in absorption and secretion of cerebrospinal fluid under resting and experimental conditions by various workers. To investigate the response of the ventricular ependyma to experimental leakage of the fluid, spinal transection was carried out in young adult Wistar rats in the lumbar region. The ependyma of the third ventricle was processed for transmission electron microscopy on the 7th post-operative day. The ependymal cells in the sham-operated control animal exhibited regional variations in respect of cilia, microvilli and in their relationship to the subjacent subependymal zone. However, most cells showed apical mitochondria and Golgi cisternae with few profiles of granular and smooth endoplasmic reticulum. Pinocytotic and dense-coated vesicles were not prominent features. In the operated rat, a few ultrastructural changes were noted. A profusion of microvilli and blebs with secondary surface modifications was characteristically seen on the ventricular face. Pinocytotic and dense-coated vesicles appeared to be consistent features. Proliferation of mitochondria, Golgi cisternae, polyribosomes and of smooth and granular endoplasmic reticulum was evident throughout the cytoplasm. The mitochondria, in many cases, presented a pleomorphic appearance with increased electron density. The above modifications in the fine structure, considered collectively, point to an increased ependymal activity. The evidences of both absorptive (presence of microvilli, pinocytotic and dense-coated vesicles) and secretory features (presence of blebs, proliferation in membrane components and in polyribosomes) within the same cell suggest its simultaneous involvement in both absorption and secretion. The observed changes may be interpreted as a compensatory attempt by the ependymal cell toward conservation and replenishment of cerebrospinal fluid.

Animals↗