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PubMed1985

Differential effects of thioridazine, clozapine and metoclopramide on the induction of adrenomedullary enzymes by apomorphine.

The induction of two adrenomedullary enzymes, ornithine decarboxylase and tyrosine hydroxylase, by apomorphine was studied in rats receiving dopamine antagonists known to by specific in their site of action. Metoclopramide, a drug that acts predominantly on the A9 dopamine system, was effective in blocking the induction of the two enzymes by apomorphine. Thioridazine and clozapine, two antipsychotic drugs that act preferentially on the A10 dopamine systems, did not impair this induction and possibly potentiated it. The results suggest that the site of action of apomorphine responsible for the induction of adrenomedullary ornithine decarboxylase and tyrosine hydroxylase is located in the striatum.

Adrenal Medulla↗
PubMed1964

THERAPY OF CHLORPROMAZINE MELANOSIS: A PRELIMINARY REPORT.

Melanosis observed in association with prolonged chlorpromazine therapy has become a serious problem in mental institutions. Skin pigmentation has produced an appearance which is cosmetically undesirable. Ocular deposits have caused visual impairment. Diffuse visceral involvement has been accompanied by functional disturbances of the involved organs.Withholding chlorpromazine did not diminish the pigment deposits already present in eight patients with chlorpromazine-induced melanosis. Therefore therapy for existing cases and means of preventing this side effect were investigated. A method of blocking melanin synthesis by depressing tyrosinase activity was devised. A copperchelating agent, D-penicillamine, was administered for a period of four weeks (300 mg. three times daily for six days each week, with mineral supplement substituted on the seventh day). Four of six days patients thus treated improved markedly as evidenced by diminution of skin pigmentation. Urinary copper excretion was substantially increased during the trial period. An alternative method of treatment designed to stimulate melatonin production by the pineal gland was employed. Two patients were kept in darkness for a period of four weeks. One improved markedly, the other only slightly.

Body Fluids↗
PubMed2006

PCR detection of foodborne bacteria producing the biogenic amines histamine, tyramine, putrescine, and cadaverine.

This study describes an easy PCR method for the detection of foodborne bacteria that potentially produce histamine, tyramine, putrescine, and cadaverine. Synthetic oligonucleotide pairs for the specific detection of the gene coding for each group of bacterial histidine, tyrosine, ornithine, or lysine decarboxylases were designed. Under the conditions used in this study, the assay yielded fragments of 372 and 531 bp from histidine decarboxylase-encoding genes, a 825-bp fragment from tyrosine decarboxylases, fragments of 624 and 1,440 bp from ornithine decarboxylases, and 1,098- and 1,185-bp fragments from lysine decarboxylases. This is the first PCR method for detection of cadaverine-producing bacteria. The method was successfully applied to several biogenic amine-producing bacterial strains.

Bacteriological Techniques↗
PubMed1984

Monosodium glutamate lesions in rat hypothalamus studied by immunohistochemistry for gonadotropin releasing hormone, neurotensin, tyrosine hydroxylase, and glutamic acid decarboxylase and by autoradiography for [3H] estradiol.

Adult male and female rats treated neonatally with monosodium glutamate (MSG) exhibit lesions in the arcuate nucleus of the hypothalamus. Immunohistochemical analysis of the distribution of tyrosine hydroxylase (TH), glutamic acid decarboxylase (GAD), neurotensin (NT) and gonadotropin-releasing hormone (GnRH) reveals substantial destructions of tuberoinfundibular dopamine and NT systems accompanied by a marked reduction of immunoreactivity in the median eminence. GAD immunoreactivity in the arcuate nucleus and median eminence is greatly reduced, while GnRH containing structures in the mediobasal hypothalamus are not noticeably affected. Evaluation of autoradiograms after intravenously administered [3H] estradiol in the ventral hypothalamus indicate an almost complete loss of target neurons in the arcuate nucleus but not in the nearby ventromedial nucleus. The results suggest that: (a) NT- and dopamine-containing neurons of the arcuate nucleus project to the median eminence via tuberoinfundibular NT and dopaminergic pathways; (b) GABA in the median eminence originates to a major extent from neurons of the arcuate nucleus through a tuberoinfundibular GABAergic system; (c) GnRH is produced in the rat outside the arcuate nucleus; (d) the MSG-induced lesion in the basal tuberal region abolishes or strongly diminishes estradiol target neurons in the arcuate nucleus.

Animals↗
PubMed2001

The presence of thyrogastric antibodies in first degree relatives of type 1 diabetic patients is associated with age and proband antibody status.

A quarter of type 1 diabetic patients have thyrogastric autoantibodies (thyroid peroxidase and gastric parietal cell antibodies). Clinical, immune, and genetic risk factors help predict antibody status. First degree relatives of these patients may also frequently exhibit these antibodies. We assessed the prevalence of thyrogastric antibodies and dysfunction in first degree relatives in relation to age, gender, human leukocyte antigen-DQ type, beta-cell antibody (islet cell, glutamic acid decarboxylase-65, and tyrosine phosphatase antibodies), and proband thyrogastric antibody status. Sera from 272 type 1 diabetic patients (116 men and 156 women; mean age, 27 +/- 18 yr; duration, 10 +/- 9 y), 397 first degree relatives (192 men and 205 women; parents/siblings/offspring, 48/222/127; age, 22 +/- 10 yr), and 100 healthy controls were tested for islet cell antibodies and gastric parietal cell antibodies by indirect immunofluorescence and for tyrosine phosphatase, glutamic acid decarboxylase-65, and thyroid peroxidase antibodies by radiobinding assays. Glutamic acid decarboxylase-65 antibodies were present in 68% and 5%, islet cell antibodies were present in 36% and 2.5%, tyrosine phosphatase antibodies were present in 45% and 0.5%, thyroid peroxidase antibodies were present in 21% and 4.5%, and gastric parietal cell antibodies were present in 18% and 11% of diabetic patients and relatives, respectively. The presence of thyroid peroxidase antibodies in relatives was determined by age (beta = 0.22; P = 0.0001) and proband thyroid peroxidase antibodies status (beta = -2.6; P = 0.002; odds ratio = 11.1). Gastric parietal cell antibody positivity in relatives was associated with age (beta = 0.04; P = 0.026). Gastric parietal cell antibody-positive compared with gastric parietal cell antibody-negative relatives were more likely to have gastric parietal cell antibody-positive probands (P = 0.01; odds ratio = 3.0). beta-Cell antibody status and human leukocyte antigen-DQ type did not influence thyrogastric antibody status in relatives. (Sub)clinical dysthyroidism was found in 3%, iron deficiency anemia was present in 12% (26% gastric parietal cell antibody-positive and 9% gastric parietal cell antibody-negative subjects; P = 0.009), and pernicious anemia was found in 0.5% (5% gastric parietal cell antibody-positive and 0% gastric parietal cell antibody-negative subjects; P = 0.012) of relatives. They had less thyroid dysfunction (P < 0.0001) and pernicious anemia (P = 0.018) than diabetic probands. In conclusion, thyrogastric antibodies and dysfunction are more prevalent in type 1 diabetic patients than in first degree relatives. The presence of these antibodies in relatives is associated with age and proband antibody status, but not with beta-cell antibodies or human leukocyte antigen-DQ type.

Adult↗
PubMed1992

Dehydroepiandrosterone: antiglucocorticoid action in mice.

The acute effect of dehydroepiandrosterone (DHEA) and its conjugate, DHEA-sulfate (DHEA-S) on glucocorticoid action was tested in vivo using male Swiss-Webster mice. The authors found that DHEA and DHEA-S significantly inhibited induction of hepatic tyrosine aminotransferase activity, although the former was more potent. This inhibition was dose- and time-dependent and was not demonstrable with other steroids. The same inhibitory effect of DHEA was seen with kidney tyrosine aminotransferase induction, as well as with liver and kidney ornithine decarboxylase enzyme activity, another glucocorticoid-induced enzyme. The conclusion is that DHEA acts acutely as an antiglucocorticoid and exerts its effect in different glucocorticoid-sensitive systems.

Adrenalectomy↗
PubMed1996

Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced ornithine decarboxylase activity by genistein, a tyrosine kinase inhibitor.

The effects of the protein tyrosine kinase inhibitor genistein on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ornithine decarboxylase (ODC) activity in monkey kidney epithelial CV-1 cells were determined. CV-1 cells were pretreated with genistein for 2 hr before treatment with 100 nM TPA. ODC activity was determined 9 hr after TPA treatment. Genistein inhibited TPA-induced ODC activity at 0.1, 1, 10, 25, 50, 100, 200, and 400 microM by 0%, 0%, 42%, 59%, 62%, 81%, 91%, and 100%, respectively (IC50 = 20 microM). Genistein inhibited TPA-induced mitogen-activated protein kinase (MAPK) tyrosine phosphorylation and the accumulation of steady state levels of ODC mRNA at 400 microM but not at 25 microM. Genistein, at 25 microM, did not alter the TPA-induced phosphorylation of p90 ribosomal S6 kinase but caused a approximately 50% decrease of the TPA-induced phosphorylation of p70 S6 kinase (p70S6K), a protein kinase involved in the control of translational efficiency. Taken together, these data indicate that genistein may inhibit TPA-induced ODC activity at the transcriptional and translational levels through the inhibition of MAPK and p70S6K activation, respectively. The regulation of MAPK and p70S6K may be mediated through different protein tyrosine kinases that have differential sensitivity to genistein.

Animals↗