Analysis of coal ash samples from thermal power plants of India for their gallium content using NAA and EDXRF techniques.

Coal fly ash (CFA) is an important secondary source for the recovery of gallium (Ga) which has a high potential for its wide applications in many strategic fields such as cellular communications and direct broadcast satellite. Various coal fly and bottom ash samples obtained from thermal power plants located in different parts of India were investigated for their gallium content using NAA and EDXRF techniques. The concentration of gallium in NIST SRM 1633b CFA is not available in NIST certificate and hence was established using k based IM-NAA method along with the other certified elements like As, Ce, Co, Eu, Fe, K etc.

Single electroconvulsive shock and dopamine autoreceptors.

Dopamine (DA) auto receptor down regulation has been suggested to mediate the therapeutic effect of antidepressant treatments including electroconvulsive therapy (ECT). Suggestion has also been made that a single ECT may have antidepressant potential via such a mechanism. The present study was therefore conducted to assess the effects ill a single electroconvulsive shock (ECS) on dopamine auto receptors in the rat brain.

Prostaglandins can modify gamma-radiation and chemical induced cytotoxicity and genetic damage in vitro and in vivo.

The effect of prostaglandin E1, E2, and F2 alpha on gamma-radiation, benzo(a)pyrene and diphenylhydantoin-induced cytotoxicity in vivo and genotoxicity in vitro was investigated. Prostaglandin E1 prevented both cytotoxic and genotoxic actions of all the three agents, where as both PGE2 and PGF2 alpha were ineffective. In fact, it was seen that both PGE2 and PGF2 alpha are genotoxic by themselves.

Dopaminergic Effects of Repeated Electroconvulsive Shocks.

Dopamine (DA) autoreceptor and postsynaptic receptor changes following repeated electroconvulsive shocks (ECS) were investigated in rats using the indices of low- and high-dose apomorphine-induced motility responses. Repeated ECS produced no changes in the DA autoreceptors; however, enhanced postsynaptic receptor-mediated responses were observed, suggesting increased sensitivity of the DA postsynaptic receptors.

Vitamin A can prevent genetic damage induced by benzo(a)pyrene to the bone marrow cells of mice.

Vitamin A and its analogues are now known to be of help in the prevention of cancer. One of the mechanisms by which cancer can occur is due to the damage to DNA. Hence, we have investigated the effect of vitamin A on genetic damage induced by benzo(a)pyrene, a known mutagen and co-carcinogen, to the bone marrow cells of mice.

Prostaglandins and their precursors can modify genetic damage-induced by gamma-radiation and benzo(a)pyrene.

Experiments were performed to study the effect of various prostaglandins (PGs) and their precursors, gamma-linolenic acid (GLA) and arachidonic acid (AA) on gamma-radiation and benzo (a) pyrene (BP)-induced genetic damage to the bone marrow cells of mice, using the sensitive micronucleus (MN) test. Thromboxane B2 prostaglandin E1 and GLA completely prevented BP-induced and reduced to a great degree radiation-induced genetic damage, where as PGE2, PGF2 alpha and AA were without any effect. Since GLA and AA are widely distributed in the cell membranes, and as PGs can be formed virtually in response to any type of stimulus, it is likely that GLA and PGE1 may function as endogenous anti-mutagenic chemicals.

Prostaglandins and mutagenesis: prevention and/or reversibility of genetic damage induced by benzo (a) pyrene in the bone marrow cells of mice by prostaglandin E1.

Prostaglandin E1 and thromboxane A2 (PGE1 and TXA2) have been proposed to bind to DNA, regulate gene action and prevent mutagenesis. Benzo (a) pyrene (BP) is a known mutagen and tumor promotor. BP-induced damage to the bone marrow cells of mice was prevented and/or reversed by PGE1 and by colchicine, an agent which may enhance PGE1 synthesis and TXA2 synthesis or action.

Prostaglandins and mutagenesis: modification of phenytoin induced genetic damage by prostaglandins in lymphocyte cultures.

Diphenylhydantoin (DPH) is known to cause genetic damage both in vivo and in vitro. We investigated the effect of prostaglandin E1, E2 and F2 alpha on DPH induced chromosomal aberrations in lymphocyte cultures in vitro. Prostaglandin E1 prevented and/or reversed DPH induced chromosomal aberrations, whereas PGE2 and PGF2 alpha were without inhibitory action.