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Biomedical subjects

P K Ray

Publications and source records attributed to P K Ray.

At least 73 records · Page 4Linked to original sources
PubMed1990

Studies on the genotoxicity of endosulfan, an organochlorine insecticide, in mammalian germ cells.

The genotoxic potential of endosulfan was assessed in mouse germ cells by 2 in vivo tests: the dominant lethal and the sperm shape abnormality test. At higher doses, endosulfan induced dominant lethal mutations in one mating interval (36-42 days) post treatment. A statistically significant dose-dependent increase in sperm abnormalities was observed with endosulfan treatment. At high doses the sperm count decreased up to 39%. No change in sperm motility was observed at any dose level. On the basis of the present in vivo results, it appears that endosulfan has a damaging effect on spermatogonial cells as well as on sperm morphology.

Animals↗
PubMed1990

Protection against carbon-tetrachloride-induced lymphoid organotoxicity in rats by protein A.

In a previous study we described protection of rats from carbon tetrachloride (CCl4)-induced hepatotoxicity by protein A (PA). In the present report we described protection against CCl4-induced lymphoid organotoxicity in rats by PA. Our data indicate that CCl4 administration produced a significant increase in the number of total leukocytes and polymorphs in blood, a significant decrease in leukocyte count in bone marrow, and a significant loss in weight of spleen and adrenals. In the animals receiving PA prior to and after CCl4, these values were found to be near those of controls. Histological examination revealed thymocyte depletion in thymic lobe and degenerative changes of tissue in spleen of CCl4-exposed animals. PA treatment to CCl4-exposed animals exhibited improvement and recovery from the damage caused by CCl4. These observations throw a new light on the field of CCl4 toxicity to lymphoid organs and their protection by PA.

Animals↗
PubMed1990

Ultrastructural features of presumptive vasopressinergic synapses in the hypothalamic magnocellular secretory nuclei of the rat.

Despite convincing physiological evidences for vasopressin (VP) autoregulation in the supraoptic (SON) and paraventricular (PVN) nuclei, the morphological demonstration of VP synapses has lagged behind. The present work investigates the possible existence of such synapses in the SON and PVN of the rat. Electron microscopy of sections immunostained with VP antibody (1:5,000) and conjugated with avidin-biotin demonstrated presynaptic terminals containing neurosecretory granule (NSG)-like bodies, 80-100 nm in diameter. The terminals formed axodendritic, axosomatic and axoaxonic synapses, though the postsynaptic elements remained largely unidentified. Other ultrastructural features of synaptic specialization were evident. The NSG-like bodies exhibited a varying and dynamic relationship to the presynaptic membrane, suggesting their involvement in synaptic mechanisms.

Animals↗
PubMed1990

Vasopressinergic axon collaterals and axon terminals in the magnocellular neurosecretory nuclei of the rat hypothalamus.

Axon collaterals emerging from the vasopressinergic neurons of the supraoptic (SON) and paraventricular (PVN) nuclei and recurving back towards their respective nuclei have been previously reported. Since such axon collaterals can play a role in the neuromodulation of SON and PVN, these nuclei have been further investigated immunohistochemically under the light and electron microscope. The PAP technique, using a commercial antibody, was employed. Vasopressin-positive axon collaterals were seen to recurve towards their nuclei of origin. In the latter, vasopressinergic intrinsic neurons were also observed. Under the electron microscope, axon terminals containing vasopressin-immunoreactive neurosecretory granules were noted. Such terminals presumably arise from the vasopressin-positive recurrent axon collaterals or from the intrinsic neurons for the purpose of neuromodulation within the SON and PVN.

Animals↗
PubMed1990

Protein A induced abrogation of cyclophosphamide toxicity is associated with concomitant potentiation of immune function of host.

This report confirms our previous observation that protein A (PA) of Staphylococcus aureus Cowan I reduces the cyclophosphamide (Cy) induced toxicity. PA treated animals recover quickly from the toxic effects of Cy. We have exhaustively studied the role of specific and nonspecific immunity in the protection of the animals. It was observed that PA helped the animals in the accelerated regeneration of leukocytes of blood (p less than 0.001) and different lymphoid organs like thymus (p less than 0.001), spleen (p less than 0.01) and bone marrow (p less than 0.01). Increased number and function of macrophages was also observed in PA (p less than 0.001) and PA+Cy (p less than 0.001) groups. PA, on one hand enhanced the cell mediated immunity while suppressed the humoral immunity as was assessed by increase in delayed type hypersensitivity response (p less than 0.001) and decreased in plaque forming cells (p less than 0.001), EAC-rosettes (p less than 0.001), hemagglutination (p less than 0.001) and hemolysin titre (p less than 0.05). On the basis of above observations we propose that the immunomodulatory activity of PA helped the animals to remain alive in two ways- (1) by early generation of the cells depleted by the Cy thus helping animals to repair the damaged immune system and fast clearance of the toxic metabolites of Cy (2) by temporarily suppressing the cells responsible for humoral immunity which are more susceptible to Cy metabolites.

Adjuvants, Immunologic↗
PubMed1990

Effect of in utero exposure to hexachlorocyclohexane on the developing immune system of mice.

Gestational exposure to 10 and 100 mg/kg body weight (m.b.w.) hexachlorocyclohexane throughout the gestation period was done to Swiss albino mice. HCH (alpha, beta and gamma isomers) residue analysis in pups showed a higher contamination in the lymphoid organs (Spleen, Thymus and Kidney) than liver in dose dependent manner. Immune functions of the offsprings of these dams along with the offsprings of vehicle treated or untreated control dams were assessed using selected parameters of both the cellular and humoral immune responses. The delayed hypersensitivity (DTH) response to sheep erythrocytes (SRBC) was significantly higher (p less than 0.01) in pups of the dams exposed to 10 mg/kg b.w. HCH and significantly impaired in pups of the dams exposed to 100 mg/kg m.b.w. HCH as compared to controls. Mitogenic responsiveness of the spleen cells in response to Concanavalin A (Con A) and Lipopolysaccharide (LPS) was almost two fold and eight fold higher respectively and antibody response to SRBC, as measured by plaque forming cells (PFC) assay was two fold higher (p less than 0.001) in pups exposed to 10 mg/kg HCH. However, 100 mg/kg m.b.w. HCH did not affect either mitogenic response or PFC response of the pups. The results, therefore, suggest that lower dose of HCH is capable of modulating the development and function of developing immune system possibly by modulating the functional organization of the T-cell populations.

Animals↗
PubMed1990

Hypertension and myocarditis in rabbits exposed to hexachlorocyclohexane and endosulfan.

Male albino rabbits were exposed to the organochlorinated pesticides hexachlorocyclohexane (HCH) and endosulfan (2.5 and 5.0 mg/kg, ip) twice a week for 12 mo. The mean body weight of the rabbits at 12 mo was lower than that of the controls. There was rise in blood pressure and heart rate. Electrocardiograms (ECG) in both the exposed groups showed increases in PR, QT and RR intervals. Extensive myocardial damage was recorded with marked degeneration of muscle fibers vacuolization and leucocytic infiltration. Adrenals had thickened capsules and hyperplasia of cortical cells. Both pesticides produced significant increases (p less than 0.001) of 11-hydroxycortisone at all time intervals. Hypertension and myocarditis occurred in rabbits exposed to HCH and endosulfan.

Adrenal Glands↗
PubMed1990

Vasopressinergic neurons and the associated blood vessels in the rat anterior hypothalamus: an immunohistochemical study.

The paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamic neurosecretory system have been extensively investigated by many workers. The functional aspects of vasopressin secretion (elaborated by the PVN and SON neurons) in relation to the vasculature of the anterior hypothalamus are also well documented. However, the available data concerning vasopressin (VP) functions are largely based on physiological studies. Corroborative morphological correlation with regard to this has received little attention. The present report elucidates the intricate anatomical relationships between the VP-neurons and the adjoining capillaries in the rat anterior hypothalamus. A peroxidase-antiperoxidase (PAP) immunocytochemical study, using a commercial VP antibody, was carried out for this purpose. The observations are interpreted from a functional standpoint. VP-immunostained elements, i.e. the somata and the processes (mainly dendrites), were localized (i) close to the wall, (ii) on the endothelium, and (iii) occasionally, in the lumen of the hypothalamic capillaries. The findings provide immunocytochemical evidence that the vasopressinergic elements are in direct relationship with the hypothalamic vasculature. This raises some interesting possibilities for the former to be involved in: (i) affecting the permeability of the blood-brain barrier for transport of various nutrient substances (important in aging and Alzheimer's disease), (ii) inducing an alteration in the water permeability of the brain vessels on which depends the precise adjustment of brain water content and of brain volume (fundamental to normal functioning of the brain), and (iii) serving as osmoreceptors of the blood flowing through the capillaries and thus providing a feedback mechanism for VP modulation.

Animals↗
PubMed1990

Vasopressinergic neurons in periependymal and periventricular areas of the rostral third ventricle of the rat.

On the lateral wall of the rostral third ventricle, an area separates the ependyma from the neurosecretory PVN neurons. Since VP from the latter discharges into the vasculature, the above area may be regarded as constituting an interface between the ventricular and vascular compartments of the CNS. As VP release into the two compartments is integrated, the interface region has been explored for possible existence of a neural infrastructure that would allow such an integration. Immunohistochemical staining for VP following colchicine treatment reveals the presence of an elaborate vasopressinergic network in the interface region that is divisible into a medial periependymal and a lateral periventricular area. A closer examination indicates that the ependymal, periependymal, periventricular and PVN areas (in that order medio-laterally) are all interconnected through this network. The medial area appears to be receptive in nature, while the connectivity of the lateral area points to an effector function. All in all, such a neural network would provide a sound morphological basis for integration of neuroendocrine mechanisms modulating VP release into the ventricular and vascular compartments of the CNS.

Animals↗
PubMed1989

Modulation of benzene toxicity by polyinosinic-polycytidilic acid, an interferon inducer.

Repeated intraperitoneal administration of benzene (1.0 ml/kg body wt.) for 3 days produced leucopenia, lymphocytopenia and significantly decreased body wt. (P less than 0.001) and organ weights of thymus (P less than 0.001) and spleen (P less than 0.001) in female albino rats. Total iron content, lipid peroxidation and superoxide dismutase activity of the liver and bone marrow were significantly increased as a result of benzene exposure. Low molecular weight (LMW) bleomycin detectable iron content was accumulated in bone marrow, whereas hepatic LMW iron was not detectable after benzene intoxication to rats. Prior administration of single dose (250 micrograms/100 g body wt.) of Poly IC, an interferon inducer with immunomodulating potential was found to be ameliorate some of the adverse effects of benzene as well as restoration of hepatic architecture histologically. Superoxide dismutase activity, lipid peroxidation, total iron content and LMW iron content (bone marrow) were normalised. Pretreatment of animals with Poly IC was able to enhance the SRBC antibody titre in benzene-treated animals. This study suggests that the beneficial effects of Poly IC in the amelioration of the acute toxicity of benzene has clinical significance.

Animals↗
PubMed1989

Investigation of correlation between physiochemical properties of metals and their toxicity to the water flea Daphnia magna Straus.

Twenty-three metal ions were tested and ranked in terms of decrease in immobilization (EC50) of Daphnia magna Straus. The 48-hr EC50 values (mg/liter) of metal ions were Hg2+, 0.0052; Ag1+, 0.01; Cu2+, 0.093; Zn2+, 0.56; Co2+, 1.49; Cr6+, 1.79; Cd2+, 1.88; Be2+, 2.82; Pb2+, 3.61; As3+, 6.23; Fe2+, 7.20; Ni2+, 7.29; Mn2+, 8.28; Sn2+, 21.56; Ba2+, 32.00; Al3+, 59.60; W6+, 89.39; Sr2+, 94.00; K1+, 141.46; Mg2+, 343.56; Na1+, 420.60; and Sb3+, 423.45. The 48-hr EC50 values of 23 metal ions were transformed to their corresponding negative logarithms of molarity (as pM). Correlation coefficients (r) for more than 35 physiochemical properties of metals or metal ions and acute toxicity values (as pM) were examined by linear regression analysis. The negative logarithm of the solubility product constant of metal sulfide (pKsp), equilibrium constants of amino acids and of EDTA, nucleotide base, electronegativity, electrode potential, melting point, thermal properties of metals, and other physiochemical parameters were significantly correlated with toxicity for D. magna. The order of toxicity of metal ions has been presented and discussed. Correlation between toxicity and physiochemical properties of inorganic substances may be useful in predicting toxicity to various biologically important organisms.

Animals↗
PubMed1989

Protein A protects mice from depletion of biotransformation enzymes and mortality induced by Salmonella typhimurium endotoxin.

Changes in hepatic microsomal mixed-function oxidase enzyme levels (aniline hydroxylase, aminopyrine demethylase, glutathione S-transferase), glutathione content, total sulphydryl content, and plasma enzyme levels of aspartate transaminase, alanine transaminase and alkaline phosphatase were studied in male Swiss albino mice exposed to Salmonella typhimurium endotoxin (50-150 micrograms per mouse, LC50 141.82 micrograms). Animals exposed to the same dose of endotoxin but pretreated with protein A of Staphylococcus aureus (5 micrograms/per mouse) protected the animals from both mortality and depletion of biotransformation enzymes.

Alanine Transaminase↗
PubMed1988

Protection against carbon tetrachloride-induced hepatotoxicity by protein A.

Protection from carbon tetrachloride (CCL4)-induced hepatotoxicity by protein A was assessed histologically in rats. Carbon tetrachloride exposure produced swollen, vacuolated and necrotic cells in the centrilobular region of the hepatocyte in rats. Animals given protein A prior to and during CCL1 treatment showed a complete absence of hepatic lesions. Our study showed that protein A, a potent immunomodulator, has the potential to reduce liver injury caused by carbon tetrachloride, a known hepatotoxin in the rat.

Animals↗
PubMed1988

A study of nerve conduction velocity, late responses and neuromuscular synapse functions in organophosphate workers in India.

To study the effect of occupational organophosphate exposure on neuromuscular function, 24 workers exposed to fenthion [0,0-dimethyl-0(4-methyl mercapto-3 methyl phenyl)phosphorothioate], whose mean age was 31.7 years (range 22-50) and mean duration of exposure to fenthion 8.5 years (range 1-19) were subjected to detailed clinical and neurophysiological evaluation after spraying. The neurophysiological tests included motor and sensory nerve conduction velocity; F response, H reflex and electromyographic neuromuscular synapse testing. Fenthion exposure was monitored by serum acetyl cholinesterase (AchE) levels. The observations were repeated after withdrawing the workers from fenthion exposure for 3 weeks to study the reversibility of the observed changes. There was no clinical evidence of peripheral neuropathy or muscle weakness. However, peroneal motor conduction velocity (p less than 0.05) terminal motor latency of median (p less than 0.1), and peroneal nerve (p less than 0.05); F minimal latency and H reflex latency (p less than 0.01) were significantly affected. Twenty-nine per cent of workers had repetitive muscle activity. Serum AchE levels also showed significant changes (p less than 0.01). The clinical significance of these subtle neurophysiological changes requires further investigation and follow-up.

Acetylcholinesterase↗