Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aldehyde-resistant, diaminobenzidine-stained endogenous peroxidases form ideal markers for the biochemical endpoints of hormone stimulation and differentiation of certain mammalian cells and tissues. The lactoperoxidase (LPO)-type of endogenous peroxidases are synthesized by the acinar cells of the salivary, Harderian, lacrimal and mammary glands and are present in their secretions. These LPO-type enzymes, that are inhibited by cyanide and aminotriazole, appear to operate extracellularly as bactericidal agents in milk and in other biological fluids. In the mammary gland, lactoperoxidase is a consistent marker enzyme for differentiated acinar cells engaged in lactogenesis. Myeloperoxidase (MPO)-type endogenous peroxidases are prominent markers for the GERL endomembrane system and differentiated lysosomes in certain cells of the reticuloendothelial system and phagocytes. MPO is prominent within eosinophils, peritoneal macrophages and in Kupffer cells. The MPO-type endogenous peroxidases function primarily within lysosomes as bactericidal agents. Thyroid peroxidase (TPO) is relegated to the cisternae of the granular endoplasmic reticulum and Golgi apparatus, to apical cytoplasmic vesicles and to the luminar cell membrane surface of acinar cells. The enzyme is probably activated at release and functions both in the organification reaction (T leads to To) and in the biosynthesis of thyroxine. Thyroid stimulating hormone (TSH) appears to play a key role in the regulation of TPO levels and activity in the thyroid gland. Certain tissues displaying growth-dependency on estrogen (i.e., uterus, cervix, vagina and the DMBA-induced rat mammary tumor) synthesize and secrete endogenous peroxidase into their lumina. These enzymes serve as important marker proteins of estrogen action, in that they occur distal to the binding of estrogen to its receptor protein. Estrogen antagonists, particularly CI-628 (Parke-Davis) and Nafoxidine (Upjohn) that appear to function through the estrogen receptor mechanism, also induce synthesis of the reproductive tract endogenous peroxidase but inhibit growth of these tissues. Progesterone antagonizes the synthesis of the reproductive tract peroxidases and inhibits growth of the tissues as well, in part, through the reduction of the cytosol estrogen receptor protein. Endogenous peroxidase activity appears to represent a reliable marker for rodent breast cancer tissues displaying dependency for estrogen and is of potential interest as a diagnostic marker protein in human breast cancer. Rat uterine peroxidase (UP) has been investigated by microelectrophoretic techniques. The molecular weight of UP has been determined in the range of 100,000 by using polyacrylamide gradient gels in the absence and presence of nonionic and anionic detergents. The isoelectric point of UP is located between pH 4.5 and 5.9. Employing the two-dimensional combination of isoelectric focusing and gel gradient electrophoresis, UP was separated into two subunits, one having a molecular weight of 70,000, the other less than 20,000.
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PMID:Mammalian endogenous peroxidases as cellular markers and as biosynthetic endpoints of hormone-mediated activity: viewpoint from cytochemistry. 22 20

Uterine peroxidase enzyme activity has been studied as a marker for estrogen action in the uterus to help clarify the mechanism of estrogen action and its modulation by antiestrogens and progestins. Estrogen-induced increases in peroxidase were found to closely parallel increases in uterine weight and DNA content in the castrate rat. In the cycling female rat, uterine peroxidase levels were highest during proestrus and estrus and the lower levels of metestrous and diestrous uteri could be raised to estrous levels by administration of estrogen. However, the estrous levels were not further increased by estrogen treatment. The antiestrogen, CI628, while a very weak inducer of uterine peroxidase, is an effective antagonist of the estrogen induction of the enzyme. The prolonged duration of this CI628-effected inhibition corresponds to the prolonged depletion of cytoplasmic estrogen receptor seen with CI628 treatment. Progesterone, R5020 and norethindrone were also found to be effective antagonists of estrogen-induced uterine peroxidase. Medrogestone and clogestrone, less potent progestins in the rat, were also less effective antagonists of peroxidase induction. Since progesterone was found to inhibit peroxidase induction due to both estrone and diethylstilbestrol, as well as estradiol, it is considered unlikely that this antagonism relates to progestin-induced increases in uterine 17 beta-hydroxysteroid dehydrogenase. Rather, it is proposed that progestins, acting through progestin receptor, may have a more direct role, possibly acting at the level of the genome to repress the expression of estrogen-induced products.
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PMID:Steroid hormone regulations of uterine peroxidase activity. 57 50

Progesterone (P)-induced PRL secretion in estradiol (E)-primed monkeys is not due to direct pituitary stimulation, because lactotropes do not express progestin receptors (PR). However, the hypothalamus, particularly the tuberoinfundibular dopaminergic system (TIDA), plays a major role in the regulation of PRL secretion. To determine whether hypothalamic dopamine neurons are progestin target cells, the colocalization of PR and tyrosine hydroxylase (TH), a phenotypic marker of dopaminergic neurons, was examined with double immunocytochemistry. Two methods for visualizing the antigens were applied; the first was a dual peroxidase method, and the second was a peroxidase-alkaline phosphatase method. In addition, the question of whether E induces PR in dopamine neurons was explored. Spayed female monkeys were treated with empty Silastic capsules, E-filled capsules for a period of 28 days, or E capsules supplemented with P capsules for the last 14 days of E treatment. Only the E- plus P-treated monkeys exhibited an increase in serum PRL during the P treatment period. Frontal sections at the level of the optic chiasm and arcuate nucleus were examined for the colocalization of TH and PR. After E treatment, hypothalamic PR-positive cells increased in both intensity and number. Neurons expressing both TH and PR were detected in the rostral hypothalamus, lateral to the third ventricle (A11-rostral) and in a discrete subventricular population (A11-subvent). The lateral population continued caudally (A11-caudal). The A11-subvent population exhibited little steroid regulation. Of the remaining A11 TH neurons, approximately 20% exhibited PR in the spayed and E-treated groups. Addition of P doubled the percentage of PR-containing TH neurons in this group. Although very few TH-positive neurons in the ventral arcuate nucleus contained PR (A12-ventral), many double labeled neurons were observed in the dorsal arcuate region (A12-dorsal). Ventral arcuate TIDA neurons were not regulated by steroids, but E plus P increased PR expression in A12-dorsal. Double labeled cells were rarely seen in the zona incerta (A13) or the emerging ventral tegmental area (A10). In summary, P probably does not act directly on ventral arcuate TIDA neurons to stimulate PRL secretion. However, the frequency of PR-positive dopamine neurons in the A11-rostral, A11-caudal, and A12-dorsal groups increased with E and P treatment. Therefore, the contribution of the PR-positive periventricular dopamine neurons to progestin-stimulated PRL secretion may be important.
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PMID:Immunocytochemical colocalization of hypothalamic progestin receptors and tyrosine hydroxylase in steroid-treated monkeys. 135 39

In our previous study, a drastic change in terminal saccharides of glycoconjugates of the hamster zona pellucida associated with oocyte maturation was observed using light microscopic methods of lectin cytochemistry. To understand the mechanism of this change, in the present study, the correlation between the cytochemical appearance of saccharide residues in the zona pellucida and nuclear maturation was examined. Immature hamsters were treated with PMSG and hCG to induce follicular development and ovulation. The animals were euthanized 0 to 26 hrs. after the injection of PMSG or 0,1,2,3,4,5,7,9 or 11 hrs. after the injection of hCG, and ovaries were dissected out, fixed, paraffin embedded and sectioned serially. Every other paraffin section was stained with hematoxylin to observe the status of nuclei and to classify follicular growth and only the fully developed preovulatory follicles were examined in experiments. The peroxidase-labelled lectin-diaminobenzidine procedure was applied to sections. The lectins employed were WGA, SBA, MPA, UEA-I, LotusA and AAA. Germinal vesicle breakdown was observed within 3 hrs. after the administration of hCG. A positive reaction of WGA, SBA or MPA for zonae pellucidae in the fully developed preovulatory follicles appeared 1 hr. after hCG injection, and remained so for the next 10 hrs. UEA-I, Lotus A and AAA reactions were negative for all of the zonae pellucidae observed. The data indicate that the synthesis of saccharide residues such as GlcNAc and GalNAc forming zona components in the follicles is not triggered by germinal vesicle breakdown.
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PMID:Appearance of lectin binding affinity to the zona pellucida during hamster oocyte maturation. 174 97

We performed light microscopic immunocytochemical observations of the localization of catechol-O-methyltransferase (COMT) in rat uterus, using a rabbit anti-rat serum specific for the soluble form of rat liver COMT, biotinylated goat anti-rabbit immunoglobulin, and peroxidase conjugated with streptavidin. In the non-pregnant rat, COMT was minimal but detectable in the uterine luminal and glandular epithelium, with greater amounts present in uteri from rats in estrus than those in diestrus. In early pregnancy a robust accumulation of COMT was observed in the luminal epithelium. To more precisely define both the timing and the factors contributing to the appearance of COMT, uteri were examined on Days 1-5 in pregnant and pseudopregnant rats. Accumulation of COMT in the luminal epithelium was observed by Day 3 in uteri from pregnant and pseudopregnant rats and by Day 4 in lactating post-partum rats. No immunostaining of COMT was observed in uteri from non-lactating post-partum rats. Ovariectomy on Day 0 or 1 but not on Day 2 of pregnancy prevented the appearance of COMT on Day 4. Progesterone treatment immediately after ovariectomy on Day 0 or 1 of pregnancy restored the COMT.
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PMID:Induction of catechol-O-methyltransferase in the luminal epithelium of rat uterus by progesterone. 203 40

In order to clarify possible alterations of membrane-, and cytoplasma-glycoconjugates of laryngeal cancer cells in metastatic process, a histochemical study was performed on laryngeal squamous carcinoma, using seven lectins conjugated with horseradish peroxidase (HRP); PNA, UEA-I, WGA, RCA-I, DBA, SBA and MPA. The author studied 32 primary tumors and 32 corresponding metastatic tumors obtained from 32 patients and primary tumors from 8 patients without histological evidence of lymph node metastasis. None of the patients underwent irradiation or chemotherapy before operation. The specimens were provided for routine lectin histochemistry. The present study revealed some significant differences in lectin-binding as follows. Primary tumor vs. metastatic tumor: There was a significant difference in lectin-binding between primary and metastatic cancer cells. 29 (90.0%) of 32 primary tumors were positive for MPA-staining. On the other hand, 21 (65.6%) of 32 metastatic tumors were positive for MPA-staining. There was a statistically significant (p less than 0.05) difference between primary and metastatic tumors with regard to MPA-binding. Primary tumor cells tended to more bind with lectins than with metastatic tumor cells. Well-differentiated primary tumor vs. moderately differentiated primary tumor: There was a significant difference in lectin-binding between these two types of tumors. Of 15 well-differentiated primary tumors, 13 (86.7%) showed SBA binding. The percentage of SBA-binding was significantly higher in well-differentiated tumor than in moderately differentiated primary tumors (50%, 8/16). Keratinization vs. non-keratinization: There was a significant difference in lectin-binding between keratinized and non-keratinized tumor cells in both primary and metastatic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lectin histochemistry of primary and metastatic tumor cells of laryngeal cancer]. 234 78

The present study investigated some lectin affinities of human dental pulps, especially of odontoblasts and pulp cells. The materials were obtained from clinically intact teeth that were caries-free, attrition and/or abrasion-free. Mucopolysaccharide staining was carried out with applied PAS and alcian blue (AB) (pH 1.0 and 2.5). Lectins used were Con A, WGA, RCA-1, UEA-1, DBA, SBA, MPA, LFA, HPA, PNA, and GS-1, and the avidin-biotin peroxidase complex method was employed. Some specimens were tested for PNA binding after treatment with sialidase. The following results were obtained: 1) On PAS and AB staining, the pulp tissue was very weakly or borderline positive. 2) Lectin binding in odontoblasts was intensely positive with Con A, WGA, RCA-1, MPA, and LFA, but negative or very weakly positive with the other lectins examined. 3) Lectin localization in odontoblasts was localized diffusely throughout the cytoplasm. 4) On PNA staining, odontoblasts were negative, but changed to positive after treatment with sialidase. 5) Odontoblast processes showed negative or borderline staining with all lectins used in this study. 6) The pulp cells were clearly positive with Con A, MPA, LFA, RCA-1, and SBA and especially LFA showed an intense reaction with the pulp cells. 7) WGA affinity for odontoblasts was very strong but that for pulp cells was very weak. 8) Lectin binding in pulp cells was observed mainly in the processes of the cells. From the above results, it is clear that the lectin binding pattern of odontoblasts differs from that of pulp cells. The data suggest that D-mannose, N-acetyl-D-glucosamine, D-galactose, and N-acetyl-D-galactosamine residues are localized in the odontoblasts and sialic acid is localized in the pulp cells.
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PMID:[Lectin histochemical study on human dental pulp. Special reference to odontoblasts and pulp cells]. 248 77

Progesterone receptors were determined on frozen sections from 74 primary human breast tumors by an immunocytochemical assay using an indirect avidin-biotin peroxidase method. In the same tumors, cytosol estrogen (ERc) and progesterone receptors (PgRc) were determined by ligand binding assay, and nuclear estrogen (ERn) and progesterone receptors (PgRn) were determined by an immunoassay. Immunocytochemical staining was seen in 36% of tumors. It was predominantly nuclear and there was extensive cell to cell heterogeneity. When the immunocytochemical results were compared to PgRc the agreement rate was 63%, but it was 77% when compared to PgRn. About one third (38%) of PgRc positive tumors were immunocytochemically defined as negative. Thus a significant discordance exists between this immunocytochemical assay for PgR and both the conventional radioligand assay (used for PgRc) and the relatively new enzyme immunoassay (used for PgRn). However discordance rates were critically influenced by the arbitrary cutoff levels that were used to define receptor positivity in the biochemical assays. Our studies support the addition to, rather than the substitution of, immunocytochemical methods, to the conventional biochemical assays for PgR, until long-term follow-up studies of patients with PgRn and immunocytochemical PgR determinations become available.
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PMID:Progesterone receptor determination in human breast tumors by immunocytochemical and biochemical techniques. 269 Sep 73

Because of its rare occurrence in the human, the endocrinologic and receptor-related aspects of an uterine leiomyosarcoma (LMS) are poorly understood when compared to what is known of, say, human endometrial cancer. Thus, to increase our understanding, we have succeeded, by the string method, in inducing an uterine LMS in the mouse and have studied the possibility of hormonal therapy as a method of treatment. The findings of our study are enumerated as follows: 1. The induced uterine LMS had an estrogen receptor, which was confirmed by a biochemical assay and, morphologically, by a PAP (the peroxidase anti-peroxidase technique); 2. The growth of this tumor was significantly inhibited by MPA (medroxyprogesterone acetate) therapy (100 mg/kg); 3. After MPA therapy, the estrogen receptor levels were increased, especially in the nucleus; and, 4. The growth of a secondary tumor, transplanted after the initial hormone therapy, was not inhibited by the readministration of MPA. Our results suggest that this experimentally-induced uterine LMS in the mouse provides a useful means to study therapeutic treatment, and may assist in furthering our understanding of human uterine LMS and lead to finding an effective therapy.
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PMID:[Experimental study of the treatment of uterine leiomyosarcoma in the mouse with progestogen]. 297 92

By using a combination of monoclonal antibodies to progestin receptors and a double-bridge peroxidase-antiperoxidase technique, a sensitive immunocytochemical method was developed for visualizing progestin receptor immunoreactivity (PR-IR) in brains of estrogen-primed guinea pigs. PR-IR neurons were observed throughout the hypothalamus and preoptic area. They were seen in largest numbers in the arcuate nucleus, periventricular preoptic regions, medial preoptic nucleus, medial preoptic area and in the ventrolateral area of the hypothalamus. Lower numbers of PR-IR positive cells were detected in the bed nucleus of stria terminalis, paraventricular nucleus and lateral hypothalamus with scattered cells seen throughout the hypothalamus and preoptic area. The PR-IR was mostly intranuclear with lighter staining in neuronal processes. Electron microscopy confirmed the predominantly intranuclear localization and further demonstrated that the reaction product was dispersed throughout the nucleus, but not associated with the nucleolus. Few PR-IR cells were observed in the absence of estradiol priming, and the reaction product was much lighter than in the presence of estradiol. Progesterone injection was without apparent effect on intensity of the PR-IR.
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PMID:Immunocytochemical localization of estrogen-induced progestin receptors in guinea pig brain. 321 2


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