Immune complex nephritis in rats induced by long-term oral exposure to cadmium.
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Biomedical subjects
Publications and source records attributed to C Dwivedi.
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The following is a review of current concepts of prenatal detection. Transabdominal amniocentesis is recognized to be an integral adjunct to prenatal care. The analysis of cultured amniotic fluid cells collected at about 16 weeks of gestation provides in utero diagnosis of nearly all chromosomal aberration syndromes, several metabolic disorders which are due to a specific enzymic deficiency due to single gene disorders, and some multifactorial disorders, such as prenatal diagnosis of neural tube defects by estimation of alphafeto protein in amniotic fluid. Various aspects of amniocentesis are discussed.
Monoamine oxidase inhibitory and anticonvulsant properties of 2-substituted styryl-6-bromo-3-(4-ethylbenzoate/4 benzhydrazide)-4-quinazoles are studied. All styryl quinazolone esters except compound number 9 exhibited monoamine oxidase inhibitory properties during oxidative deamination of kynuramine. Corresponding hydrazides were found to have relatively higher activity. All these quinazolones were able to protect against pentylenetetrazol induced seizures. These observations in general do not prove that monoamine oxidase inhibitory properties represent the biochemical basis for the anticonvulsant activity of these compounds.
Methylmercury poisoning exhibit prominent signs and symptoms of the central nervous system. In an attempt to study the mechanism of toxicity, mercuric chloride (HgCl2) and methyl mercury chloride (CH3HgCl) were given orally by gavage and through drinking water to male albino rats. Rats were sacrificed at appropriate time and brain and diaphragm were analyzed for cholineacetyltransferase (ChAT) activity, and also examined histopathologically. Both HgCl2 and CH3HgCl given orally by gavage significantly inhibited ChAT activity which was dose related. CH3HgCl produced greater inhibition than HgCl2. CH3HgCl through drinking water also significantly inhibited brain ChAT, however rats did not drink water containing HgCl2. Both HgCl2 and CH3HgCl also inhibited ChAT when incubated in vitro with rat brain homogenates. Histopathological studies revealed neural degeneration and necrosis in the cerebrum of rats treated with these mercurials. These results indicate the possible involvement of cholinergic system during mercury intoxication.
Rats treated with cadmium developed an interstitial pneumonitis with intraalveolar hemorrhage. In the spleen there was marked germinal center formation containing reactive B-cells. Lesions of the kidneys resembled those found in cadmium poisoning in man, primarily a proliferative glomerulonephritis.
5-(4-Aminophenoxymethyl)-2-oxazolidinethiones were synthesized by the cyclization of 1-(4-aminophenoxy)-3-amino-2-propanol in the presence of potassium hydroxide and carbon disulfide. This oxazolidinethione, on reaction with suitable isothiocyanates, yielded 5-[4-(substituted thiocarbamido)phenoxymethyl]-2-oxazolidinethiones. These compounds antagonized the uterotropic effects of diethylstilbestrol in female rats and possessed approximate LD50 values of 400-greater than 800 mg/kg.
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2-(N-Arylcarboxamide)-3-substituted ethoxyindoles were synthesized by the reaction of 2-(N-arylcarboxamide)-3-hydroxyindoles, which were obtained by the cyclization of 2-carbomethoxyphenylglycine-substituted anilides. These 2-(N-arylcarboxamide)-3-substituted ethoxyindoles were evaluated for their in vitro monoamine oxidase inhibitory ability and in vivo monamine oxidase inhibitory property as evidence by reserpine reversal response. Their anticonvulsant activity also was determined against pentylenetetrazol-induced seizures. No definite correlation could be observed between chemical structure and biological activity.
Several 1-(2,4-dichloro and 2,4,5-trichlorophenoxyacetyl)-4-alkyl/arythiosemicarbazides were synthesized and characterized by their sharp melting points and elemental analyses. All substituted thiosemicarbazides protected in vitro hypoosmotic hemolysis of dog red blood cells. These thiosemicarbazides selectively inhibited nicotinamide adenine dinucleotide (NAD)-dependent oxidation of pyruvate and alpha-ketoglutarate, while NAD-independent oxidation of succinate was not affected. These compounds inhibited the activity of monamine oxidase in rat brain homogenate, and the degree of inhibition ranged from 26.5 to 89.2 percent at a final concentration of 0.03mM, with kynuramine as the substrate. Almost all thiosemicarbazides possessed anticonvulsant activity; protection against pentylenetetrazol-induced convulsions in mice ranged from 10 to 70 percent at a dose of 100 mg/kg ip. These results provided evidence of some similarity between the membrane-stabilizing property of these substituted thiosemicarbazides with their ability to exhibit selective inhibition of NAD-dependent oxidations and inhibition of monoamine oxidase. On the other hand, the anticonvulsant activity possessed by these substituted thiosemicarbazides was unrelated to their in vitro antihemolytic and enzyme inhibitory properties.
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Several 1-substituted acetyl-3-aryl carbamides selectively inhibited nicotinamide adenine dinucleotide (NAD) dependent oxidation of alpha-keotoglutarate and beta-hydroxybutyrate by rat brain homogenates. NAD-independent oxidation of succinate remained unaltered. The inhibition observed with 1-(N-acetylmorpholino)-3-(4-methylphenyl)carbamide was competitive in nature.
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