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Biomedical subjects

M Misbahuddin

Publications and source records attributed to M Misbahuddin.

12 recordsLinked to original sources
PubMed2005

Absorption and metabolism of paracetamol in rats drinking high concentration of arsenic.

The effect of chronic intake of arsenic on the plasma concentration of paracetamol in rat was investigated. Rats received saline water with or without arsenic trioxide (10 mg/kg body weight/day) by gastric gavage on every alternate day for 29 days. A single dose of paracetamol (range 10 infinity 40 mg/kg body weight) was administered by gastric gavage to both arsenic-untreated and -treated rats on 30(th) day. Rats were sacrificed after 30 min and the amounts of free paracetamol and its metabolites in plasma were estimated using isocratic reverse-phase High Performance Liquid Chromatography (HPLC). Arsenic toxicity reduced the plasma concentration of paracetamol to 53 - 65% when compared with the rats received no added arsenic. There were maximum 67.4 and 76.9% inhibitions of sulfate and cysteine conjugations of paracetamol respectively. But arsenic had no effect on glucuronide and mercapturate conjugations. Both liver and small intestine showed increased accumulation of arsenic and decreased amount of glutathione in arsenic-treated rats. This study suggests that chronic ingestion of arsenic inhibit the absorption and metabolism of paracetamol.

Acetaminophen↗
PubMed2005

Effect of hexane extract of spirulina in the removal of arsenic from isolated liver tissues of rat.

The present study was conducted to investigate whether the active compound(s) of spirulina is present in its -- alcohol extract, hexane extract, DCM extract or in their residues. In phase I the accumulation of arsenic in isolated liver tissues of rat at different incubation period (15, 30, 45 minutes) was seen. In phase II arsenic-loaded liver tissues were incubated in presence and absence of alcohol extract, alcohol extraction residues, hexane extract, hexane extraction residues, DCM extract and DCM extraction residues of spirulina respectively. The percentage removal of arsenic from liver tissues by different extracts and residues of spirulina was estimated by Atomic Absorption Spectrophotometer. In phase III arsenic-loaded liver tissues were incubated in presence and absence of different concentration of hexane extract of spirulina and the percentage removal of arsenic from liver tissues was estimated. This study showed that the accumulation of arsenic in isolated liver tissue was time dependent and highest accumulation found was 0.69 microg/g tissues after 45 minutes incubation, which was highly significant. The percentage removal of arsenic from arsenic loaded liver tissues by alcohol extract, alcohol extraction residues, hexane extract, hexane extraction residues, DCM extract, DCM extraction residues were 33.8%,4.4%,83.0%,10.2%,7.3% and 2.9%, respectively. The percentage removal of arsenic by hexane extract at the concentration of 1, 10, 100 microg were 13.2%, 29.4% and 89.7%, respectively. Among the different extracts and residues of spirulina the hexane extract causes highly significant (p<0.001) removal. In conclusion the present study suggests that the active compound(s) of spirulina is present mostly in its hexane extract.

Animals↗
PubMed1988

Stimulatory effect of vasoactive intestinal polypeptide on catecholamine secretion from isolated guinea pig adrenal chromaffin cells.

The stimulatory effect of vasoactive intestinal polypeptide (VIP) on catecholamine (CA) secretion from isolated guinea pig adrenal chromaffin cell was studied. VIP (1-10 microM) induced dose-dependent CA secretion, which was slow and continued for at least 30 min. This VIP-induced CA secretion was dependent on the presence of Ca2+ in the medium, but no significant increase in Ca2+ uptake by the cells was observed during their stimulation with VIP. Studies on the intracellular free Ca2+ level ([Ca2+]i) using fura-2 showed that acetylcholine and muscarine induced a marked increase in the [Ca2+]i, but that VIP induced only a slight increase. Thus VIP may induce CA secretion by increasing the sensitivity of the secretion of CA to Ca2+.

Adrenal Medulla↗
PubMed1988

Muscarinic stimulation of guinea pig adrenal chromaffin cells stimulates catecholamine secretion without significant increase in Ca2+ uptake.

In isolated guinea pig adrenal chromaffin cells, not only nicotine, but also muscarine stimulated catecholamine (CA) secretion, the stimulation by muscarine being the greater. The secretions of CA by muscarine and nicotine were both dependent on the presence of Ca2+ in the medium, but only the latter was associated with a rapid increase in 45Ca2+ uptake. Experiments with the fluorescent Ca2+ indicator quin 2, showed that muscarine caused an increase in cytoplasmic free Ca2+ concentration [( Ca2+]i). Moreover, the intracellular Ca2+ antagonist 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) inhibited both CA secretion and increase in [Ca2+]i induced by muscarine. These results indicate that in isolated guinea pig adrenal chromaffin cells, nicotine stimulated CA secretion by increasing Ca2+ uptake by the cells, whereas muscarine stimulated CA secretion by mobilizing Ca2+ from the intracellular pool.

Adrenal Medulla↗
PubMed1987

Stimulation by vasoactive intestinal polypeptide of catecholamine synthesis in isolated bovine adrenal chromaffin cells. Possible involvement of protein kinase C.

In isolated bovine adrenal medullary cells, vasoactive intestinal polypeptide (VIP) stimulated 14C-catecholamine synthesis from 14C-tyrosine, but not from 14C-DOPA. This stimulatory effect of VIP on 14C-catecholamine synthesis was not dependent upon extracellular Ca2+. VIP did not affect the intracellular cyclic AMP (cAMP) level. The stimulatory effect of VIP on 14C-catecholamine synthesis was additive with that of carbamylcholine, which was dependent upon extracellular Ca2+, but not with that of phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA), an activator of protein kinase C. Moreover, 1-(isoquinolinyl-sulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, inhibited not only TPA-stimulated, but also VIP-stimulated 14C-catecholamine synthesis from 14C-tyrosine. These results suggested that VIP stimulated catecholamine synthesis by activation of tyrosine hydroxylase and that protein kinase C was involved in this stimulatory mechanism.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Effects of DJ-7141, a new alpha 2-adrenoceptor agonist, on catecholamine secretion from isolated bovine adrenal medullary cells.

The effects of a newly synthesized alpha 2-adrenoceptor agonist (an imidazole derivative, DJ-7141) on catecholamine secretion from isolated bovine adrenal medullary cells were examined. DJ-7141 did not affect basal catecholamine secretion, but inhibited catecholamine secretion induced by stimulation of the nicotinic ACh receptor. This inhibitory effect of DJ-7141 was less than that of clonidine, another alpha 2-agonist. DJ-7141 also inhibited [45Ca]2+ uptake by the cells induced by nicotinic stimulation. DJ-7141 did not affect catecholamine secretion induced by high K+ concentration. Its inhibitory effect on nicotine-induced catecholamine secretion was not restored by increase in either the nicotine or Ca2+ concentration of the medium, suggesting that it interfered with the coupling between nicotinic ACh receptor stimulation and Ca2+-channel activation. The inhibitory effect of DJ-7141 seemed to be independent of its effect on alpha 2-adrenoceptors, because its effect was not antagonized by the alpha 2-adrenoceptor antagonists yohimbine and DG-5128, which both had no effect on either basal or nicotine-induced catecholamine secretion.

Adrenal Medulla↗
PubMed1986

Stimulation by vasoactive intestinal polypeptide of muscarinic receptor-mediated catecholamine secretion from isolated guinea pig adrenal medullary cells.

The effects of vasoactive intestinal polypeptide (VIP) on catecholamine (CA) secretion by isolated guinea pig adrenal medullary cells were studied. VIP (1 microM) alone induced only a slight secretion of CA, but it stimulated ACh-induced CA secretion. At concentrations of 0.01-1 microM, it stimulated muscarine-induced CA secretion, but not nicotine-induced CA secretion. It did not affect high K+ or Ca2+ ionophore-induced CA secretion. The stimulatory effect of VIP on muscarine-induced CA secretion was observed at muscarine concentrations of 2 200 microM and was detectable after 2 min incubation.

Adrenal Medulla↗
PubMed1985

Muscarinic receptor-mediated increase in cytoplasmic free Ca2+ in isolated bovine adrenal medullary cells. Effects of TMB-8 and phorbol ester TPA.

The change in cytoplasmic free calcium, [Ca2+]i in isolated bovine adrenal medullary cells during stimulation by acetylcholine (ACh) in Ca2+-free incubation medium was measured using the fluorescent Ca2+ indicator quin2. ACh (1-100 microM) caused an increase in [Ca2+]i by mobilization of Ca2+ from the intracellular pool. Nicotine (10 microM) did not increase [Ca2+]i in the absence of extracellular Ca2+. Pretreatment of the cells with atropine (10 microM) completely inhibited ACh-induced increase in [Ca2+]i, whereas pretreatment with hexamethonium (100 microM) did not. The intracellular Ca2+ antagonist 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), inhibited ACh-induced increase in [Ca2+]i. The activator of protein kinase C 12-O-tetradecanoylphorbol-13-acetate (TPA), but not its 'inactive' analog 4 alpha-phorbol-12,13-didecanoate (PDD), also inhibited ACh-induced increase in [Ca2+]i. These findings suggest that in bovine adrenal medullary cells, stimulation of muscarinic ACh receptor causes an increase in [Ca2+]i by mobilizing Ca2+ from the intracellular pool and that protein kinase C is involved in 'termination' or 'down regulation' of this response.

Acetylcholine↗