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At least 865 records · Page 48Linked to original sources

PubMed1981

Effects of pesticides on activities of enzymes and microorganisms in a clay soil.

Laboratory experiments were conducted to determine the effect of 32 pesticides applied at 2 levels on populations of microorganisms, activities of urease, dehydrogenase, phosphatase and nitrogenase in a clay loam incubated for 1 week. Results indicated that a decrease in bacterial number was observed with thiram for 2 days and stimulation with chlorpyrifos after 7 days. Some fungicides and fumigants inhibited fungal numbers for 2 days. The recovery was rapid and stimulatory effects on microbial numbers were evident in many samples. None of the pesticides inhibited soil urease drastically. Formazan formation was not suppressed vigorously by the treatments. With the exception of DD and Vorlex at a high level, none of the treatments inhibited phosphatase in the hydrolysis of p-nitrophenyl disodium orthophosphate. A temporary decrease in nitrogenase activity in acetylene (C2H2) reduction was observed with many pesticides. The low amount of pesticides applied to the clay loam is unlikely to have detrimental effects on soil microbes and the enzymes important to soil fertility.

Acetylene↗

PubMed2002

Reduction of Cr(VI) and bioaccumulation of chromium by gram positive and gram negative microorganisms not previously exposed to Cr-stress.

Resistance to Cr(VI) is usually associated with its cellular exclusion, precluding enrichment techniques for the isolation of organisms accumulating Cr(VI) via bioreduction to insoluble Cr(III). A technique was developed to screen for potential Cr(VI) reduction in approx. 2000 isolates from a coastal environment, based on the non-specific reduction of selenite and tellurite to Se0 and Te0, and reduction of tetrazolium blue to insoluble blue formazan. The most promising strains were further screened in liquid culture, giving three, which were identified by 16S rRNA sequence analysis as Bacillus pumilus, Exiguobacterium aurantiacum and Pseudomonas synxantha, all of which reduced 100 microM Cr(VI) anaerobically, without growth. The respective removal of Cr(VI) was 90% and 80% by B. pumilus and E. aurantiacum after 48 h and 80% and by P. synxantha after 192 h. With the gram positive strains Cr(VI) promoted loss of flagella and, in the case of B. pumilus, lysis of some cells, but Cr was deposited as an exocellular precipitate which was identified as containing Cr and P using energy dispersive X-ray microanalysis (EDAX). This prompted the testing of Citrobacter sp. N14 (subsequently re-assigned by 16S rRNA sequence analysis and biochemical studies as a strain of Serratia) which bioprecipitates metal cation phosphates via enzymatically-liberated phosphate. This strain reduced Cr(VI) at a rate comparable to that of P. synxantha but Cr(III) was not bioprecipitated where La(III) was removed as LaPO4, even though a similar amount of phosphate was produced in the presence of Cr(III). Since B. pumilus removed most of the Cr(VI), with the formation of cell-bound CrPO4 implicated, this suggests that this strain could have future bioprocess potential.

Bacillus↗

PubMed2002

Influence of opioid peptides on human neutrophil apoptosis and activation in vitro.

BACKGROUND: It has been shown that cells of the immune system release opioid peptides and possess receptors for them. The concentrations of opioid peptides in the peripheral circulation rapidly increase during inflammation and acute stress response. AIMS: The effect of opioid peptides Met-enkephalin (M-ENK) and beta-endorphin (beta-END) on the oxidative metabolism of normal human neutrophils and their death by apoptosis in vitro was investigated. METHODS: Isolated from peripheral blood, neutrophils were incubated in the presence or absence of 10(-6) to 10(-10) M of M-ENK and beta-END for 12 and 18 h. Apoptosis of neutrophils was determined in vitro by flow cytometric analysis of cellular DNA content and Annexin V-FITC protein binding to the cell surface. The MTT-reduction assay was employed to estimate the oxidative metabolism of neutrophils. RESULTS: Treatment with M-ENK caused a significant increase in apoptotic cells after 18 h of culture: *0 M (control) versus 10(-10) M, p < or = 0.02; **10(-10) M versus 10(-10) M, p < or = 0.02. Treatment with beta-END caused a significant increase in apoptotic cells after 12 h of culture: 0 M versus 10(-8) M, p < or = 0.03; **0 M versus 10(-10) M, p < or = 0.04. We found the significant increase in MTT reduction by neutrophils in the presence of M-ENK and beta-END both before and after the culture. However, the ability of neutrophils to reduce the MTT salt to formazan decreased significantly after the culture. CONCLUSIONS: We observed that the in vitro effect of opioid peptides on the neutrophil survival and their functional state was time and dose dependent. The presence of antioxidants in the culture medium modifies neutrophil survival.

Apoptosis↗

PubMed2006

Candida albicans and Candida dubliniensis: comparison of biofilm formation in terms of biomass and activity.

Candida albicans and C. dubliniensis are two species responsible for oral candidiasis, especially in immunocompromised patients. Microbial infection is preceded by adherence and biofilm formation. Biofilm formation represents the most common form of C. albicans in the oral cavity and is considered to be one of the most important virulence factors. In this study, the biofilm formation ability of C. dubliniensis was compared with that of C. albicans in terms of biomass (quantified using crystal violet) and activity (assessed by formazan salts formation). Both species formed heterogeneous biofilms; however, species and strain variations were seen in the quantification of biomass and activity. There was no correlation between pseudohyphae formation and biofilm formation capability.

Biofilms↗

PubMed2002

Relationship between tumor cell load and sensitivity to the cytostatic effect of two novel platinum-bile acid complexes, Bamet-D3 and Bamet-UD2.

Based on the organotropic characteristics of bile acids towards the liver and the intestine, two novel compounds of the Bamet family, containing at least one bile acid moiety bound to platinum(II), have been synthesized and their cytostatic effect compared to their ability to become accumulated in tumor cells of hepato-intestinal origin. Bamet-UD2 [cis-diammine-bis-ursodeoxycholic platinum(II)] induced a marked inhibition of cell growth, which was more marked in human hepatoblastoma HepG2 and mouse hepatoma Hepa 1-6 cells than in rat hepatoma McA-RH7777 and human colon adenocarcinoma LS 174T cells. This effect was similar to that observed for cisplatin and stronger than that previously reported for other members of this family, such as Bamet-H2 and Bamet-R2. By contrast, Bamet-D3 [(N'N'' cis-dichloro N(3-3-amminepropylammine)propyl) glycocholamide platinum (II)] was only effective in reducing growth in human hepatoblastoma HepG2 cells. Because the in vitro DNA-reactivity was approximately 5-fold higher for Bamet-D3 than for Bamet-UD2, an additional cause for the difference in their cytostatic abilities was sought, investigating the relationship between cell load and the cytostatic effect of the drugs. Drug uptake by two cell lines, Hepa 1-6 and HepG2, with different sensitivities to these compounds was measured. The cellular uptake of Bamet-D3 and Bamet-UD2 was several-fold higher than that of cisplatin. No significant difference in the amount of both drugs taken up by these cell types was found. A study on sodium-dependency and substrate specificity indicated that Hepa 1-6 cells take up Bamet-D3 and Bamet-UD2 via similar mechanism(s), whereas these compounds do not seem to share the uptake pathways in HepG2 cells. Measurement of cell viability by formazan formation from tetrazolium salts and by neutral red uptake, after short-term (6 h) exposure to the desired drug, indicated that no acute toxic effect occurs in the presence of cisplatin or Bamet-D3 in either HepG2 or Hepa 1-6 cells. By contrast, in both cell lines Bamet-UD2 induced acute cell toxicity in a dose-dependent fashion. In sum, the results indicate that tumor cells efficiently take up these two novel compounds of the Bamet family. Although the exact uptake mechanism remains unknown, it seems to be dependent on the cell type. However, the cell load does not account for the differences in the anti-proliferative properties of the drugs. The strong and promising cytostatic activity of Bamet-UD2 is additionally related to its ability, absent in Bamet-D3, to acutely alter cellular functions other than proliferation.

Animals↗

PubMed2001

Lucigenin chemiluminescence in human seminal plasma.

Seminal plasma protects spermatozoa from the detrimental effects of reactive oxygen species such as hydrogen peroxide. We investigated the lucigenin-dependent chemiluminescence in cell-free seminal plasma from andrological patients. The seminal plasma was separated from cells by centrifugation. In all seminal plasmas studied lucigenin-dependent chemiluminescence (LCL) was detected. The LCL showed a strong pH-dependence. The signal was stable if samples were stored at +4 degrees C for up to 4 days or up to 8 days at -80 degrees C. Filtration of the samples (0.45 and 0.22 microm pore size) did not lower their luminescence. The addition of superoxide dismutase (SOD) and ascorbic acid oxidase (AAO) lowered LCL nearly to baseline values while trolox and desferal showed moderate effect, whereas allopurinol had no effect. Electron paramagnetic resonance spectroscopy demonstrated ascorbyl radicals in seminal plasma. Physiological concentrations of ascorbic acid yielded SOD-inhibitable lucigenin-chemiluminescence. The nitroblue-tetrazolium assay showed that ascorbic acid in buffer solution produced formazan. Superoxide-anion radicals were not detected in seminal plasma by the spin-trap DEPMPO due to their low steady state concentration. It is concluded that in seminal plasma ascorbate reacts with molecular oxygen yielding ascorbyl radicals and superoxide anion. If lucigenin is added to seminal plasma, reducing substances present, such as ascorbate, reduce lucigenin to the corresponding radical; this radical reacts with molecular oxygen and also forms O2-. So LCL in human seminal plasma results from the autoxidation of ascorbate and the oxidation of the reduced lucigenin. While the physiological relevance of the former mechanism is unknown, the latter is an artifact.

Acridines↗

PubMedDate not supplied

Effects of 1,3,5-Trinitrobenzene on cytotoxicity and metabolic activity of type I astrocytes of rats.

1,3,5-Trinitrobenzene (TNB) is a munitions chemical that causes gliovascular lesions in the brain stem of rats similar to those produced by thiamine deficiency and nitroaromatic compounds, including m-dinitrobenzene. To identify neuropathic indices of toxicity, the effects of varying concentrations (0 to 2 mM) of TNB on cytotoxicity and cellular metabolic activity were examined using cultured astrocytes from Fischer-344 rats. The cytotoxicity was assessed by lactate dehydrogenase (LDH) leakage into the culture medium. Astrocyte metabolic activity was assessed by measuring the conversion of a tetrazolium salt to a formazan product. Additionally, the effects of oxidative stress on cellular metabolic activity were determined by varying oxygen tension via alteration of culture media depth. In vitro, the toxic concentration 50% (TC50) of TNB, which induced cell death, was 16 microM following a 24-h exposure. The concentration of TNB that reduced cellular metabolic activity by 50% was 29 microM following a 24-h exposure. Varying the depth of the culture media did not influence the cellular metabolic activity in control or TNB-treated astrocytes. These results support the hypothesis that TNB induced neurotoxicity could partially be mediated via injury to astrocytes, a major component of the blood-brain barrier.

Animals↗

PubMed1989

A comparison of two assays for the in vitro chemosensitivity testing of human acute non-lymphoblastic leukemia cells.

In vitro chemosensitivity of blast cells from 19 patients, affected by acute non-lymphocytic leukemia, to cytosine arabinoside and daunorubicin was investigated. A semiautomated P-iodonitrotetrazolium violet (INT) colorimetric assay, based on the ability of viable cells to cleave piodonitrotetrazolium violet into a red formazan derivative and a short-term antimetabolic assay based on the uptake inhibition of [3H]-thymidine were compared in terms of their ability to predict clinical outcome. Both methods were able to discriminate between sensitive and resistant patients by in vitro cytosine arabinoside testing. On the contrary the assays carried out with daunorubicin failed to predict the clinical outcome. A good correlation was demonstrated between the results of the two different methodological approaches, validating the recently described INT sensitivity test.

Adult↗

PubMed1965

LOCALIZATION OF THE SUCCINIC DEHYDROGENASE SYSTEM IN ESCHERICHIA COLI USING COMBINED TECHNIQUES OF CYTOCHEMISTRY AND ELECTRON MICROSCOPY.

The activity of the succinic dehydrogenase system was studied in Escherichia coli utilizing combined techniques of cytochemistry and electron microscopy. Organisms were incubated in a medium containing tetranitro-blue tetrazolium (TNBT) which served as an electron acceptor. Enzymatic activity, as evidenced by the deposition of aggregates of TNBT-formazan, was found associated with the site of the plasma membrane of the bacterium.

Cell Membrane↗

PubMed1965

The demonstration of the succinic dehydrogenase system in Bacillus subtilis using tetranitro--blue tetrazolium combined with techniques of electron microscopy.

Activity of the succinic dehydrogenase system was studied in Bacillus subtilis utilizing combined techniques of cytochemistry and electron microscopy. Organisms were incubated in a medium containing tetranitro-blue tetrazolium (TNBT) which served as an electron acceptor. Enzymatic activity, as evidenced by deposition of TNBT-formazan, was found on membranous organelles associated with the cytoplasmic membrane and septal plasma membrane, the nuclear area, and the plasma membrane. Flagella, approximately 190 A in diameter, with thorn-like projections protruded through the cell wall. Tangential-oblique sections of the cell wall showed many pores approximately 220 A in diameter with a center-to-center spacing of approximately 450 A.

Bacillus subtilis↗

PubMed1975

Localization of NADH oxidase on the surface of human polymorphonuclear leukocytes by a new cytochemical method.

The ultrastructural localization of NADH oxidase, a possible enzyme in the increased oxidative activity of polymorphonuclear leukocytes (PMN) during phagocytosis, was studied. A new cytochemical technique for the localization of H2O2, a product of NADH oxidase activity, was developed. Cerous ions, in the presence of peroxide, form an electron-dense precipitate. Resting and phagocytically stimulated PMN were exposed to cerous ions at pH 7.5 to demonstrate sites of NADH-dependent, cyanide-insensitive H2O2 production. Resting PMN exhibites slight activity on the plasma membrane; phagocytizing PMN had extensive deposits of reaction product localized within the phagosome and on the plasma membrane. Peroxide involvement was demonstrated by the inhibitory effect of catalase on cerium precipitation; the surface localization of the enzyme responsible was confirmed by using nonpenetrating inhibitors of enzymatic activity. A correlative study was performed with an NADH-dependent, tetrazolium-reduction system. As with cerium, formazan deposition on the surface of the cell was NADH dependent, cyanide insensitive, and stimulated by phagocytosis. Superoxide dismutase did not inhibit tetrazolium reduction, as observed cytochemically, indicating direct enzymatic dye reduction without superoxide interposition. These findings, combined with oxygen consumption studies on resting and stimulated PMN in the presence or absence of NADH, indicate that NADH oxidase is a surface enzyme in human PMN. It is internalized during phagocytosis and retains its peroxide-generating capacity within the phagocytic vacuole.

Animals↗

PubMed1980

Macrophage variants in oxygen metabolism.

Whereas phagocytic cells from normal individuals have the capacity to kill ingested bacteria and parasites, those from patients with several uncommon genetic deficiency diseases are known to be defective in bactericidal activity. Studies on neutrophils of these patients have revealed fundamental defects in their ability to reduce molecular oxygen and metabolize it to superoxide anion, hydrogen peroxide, and oxygen radicals. In the present experiments, we describe a clone of a continuous murine macrophage-like cell line, J774.16, that, upon appropriate stimulation, activates the hexose monophosphate shunt, and produces superoxide anion and hydrogen peroxide. With nitroblue tetrazolium to select against cells capable of being stimulated by phorbol myristate acetate to reduce the dye to polymer--formazan--which is toxic fot cells, we have selected for variants that are defective in oxygen metabolism. Four of these subclones have been characterized and found to be lacking in the ability (a) to generate superoxide anion, as measured by cytochrome c reduction; (b) to produce hydrogen peroxide, as measured by the ability to form complex I with cytochrome c peroxidase; and (c) to be stimulated to oxidize glucose via the hexose monophosphate shunt. These variants appear to represent a useful model for studying the molecular basis for macrophage cytocidal activity.

Animals↗

PubMed2001

Toxic effects of mitomycin-C on cultured ciliary process cells and trabecular meshwork cells.

Mitomycin-C has recently become an adjunct medication for inhibition of fibroblast proliferation in glaucoma filtering procedures. Prolonged postoperative ocular hypotony has been a frequent complication of trabeculectomy with mitomycin-C. In order to characterize the hypotony mechanism, we compared the toxic effects of mitomycin-C on cultured rabbit ciliary process cells and trabecular meshwork cells. The results indicate that mitomycin-C has a more marked effect on ciliary process cells on 3H-thymidine uptake than on trabecular meshwork cells at concentrations ranging from 10(-1) to 10(-5) mg/ml after 3-, 5- and 60-min treatment, respectively. The living cells after mitomycin-C treatment were estimated with MTT assay that was converted tetrazolium dye of living cells only into insoluble purple formazan crystals within mitochondria. In the presence of mitomycin-C for 3, 5, and 60 min, the cellular MTT values in ciliary process cells were more decreased than in trabecular meshwork cells. Depolarization of the trabecular meshwork cells with 50 mM KCl led to an increase in intracellular calcium concentration, whereas application of mitomycin-C at 10(-3) mg/ml resulted in decrease of KCl-induced intracellular calcium increase. Mitomycin-C (10(-3) mg/ml) decreased cAMP concentration in ciliary process cells following 3- and 5-min treatment; however, it did not significantly affect the cellular cAMP concentration after only a 1-min exposure. Mitomycin-induced marked ladder pattern of DNA fragmentation was observed in ciliary process tissues after treatment with 10(-1) mg/ml of mitomycin-C for 3 and 5 min. However, the DNA pattern in trabecular meshwork tissues was not obviously affected by mitomycin-C. These findings from our results indicate that mitomycin-induced ocular hypotony may result from damage to both ciliary process and trabecular meshwork tissues.

Animals↗

PubMed2001

Induction of cellular toxicity in cultured porcine corneal keratocytes by endothelin-1.

The effect of endothelin-1 (ET-1) on corneal cells is not well understood. We investigated the biochemical changes of cultured porcine corneal keratocytes under exposure to ET-1. The results indicate that ET-1 has remarkable effects to inhibit corneal keratocytes on 3H-thymidine, 3H-leucine, 3H-uridine uptakes and cellular migration. It is in a dose-dependent manner at concentrations ranging from 10(-7) M to 10(-9) M. The 50% inhibitory dose (ID50) for ET-1, as measured by 3H-thymidine uptake, 3H-uridine uptake and 3H-leucine uptake, were 10(-7) M, 10(-0.52) M and 10(-11.8) M, respectively. The dead and living cells were estimated with MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay that was converted tetrazolium dye of living cells only into insoluble purple formazan crystals within mitochondria. In the presence of ET-1, the cellular MTT values were also decreased. The ID50 for ET-1 with cell migration assay and MTT assay were measured at 10(-7.86) M and 10(-5.1) M. Endothelin-1 (10(-6) M) promptly changed cellular morphology and attenuated adhesion observed with laser scanning cytometer. Endothelin-1-induced characteristic apoptosis cells were observed using a TUNEL assay that detected fragmented DNA of apoptosis. Western blot assay revealed that endothelin-1 induced proteolysis and decreased in fibronectin protein. These findings indicate that endothelin-1 may lead keratocytes to death resulting from induction of apoptosis and functional loss.

Animals↗

PubMed2006

Corneal toxicity of cell-penetrating peptides that inhibit Herpes simplex virus entry.

Cell-penetrating peptides (CPPs) inhibit Herpes simplex virus entry at low micromolar concentrations and may be useful either as prophylactic or therapeutic agents for herpetic keratitis. The aim of this study was to assess the in vitro and in vivo toxicity of three CPPs-EB, TAT-C, and HOM (penetratin)-for the cornea. Incubation of primary (HK320) or immortalized (THK320) human keratocytes with the EB peptide (up to 100 microM), bHOMd (up to 200 microM), or TAT-C (up to 400 microM) resulted in no evidence of toxicity using a formazan dye-reduction assay. Similar results were obtained with a human trabecular meshwork cell line (TM-1), primary human foreskin fibroblasts (DP-9), Vero, and HeLa cells with EB and TATC. The bHOMd peptide showed some toxicity in Vero and HeLa cells, with CC50 values of 70 and 93 microM, respectively. The EB peptide did not inhibit macromolecular synthesis in Vero cells at concentrations below 150 microM, although cell proliferation was blocked at concentrations of EB above 50 microM. In vivo toxicity was assessed by applying peptides in Dulbecco's modified Eagle's medium to the cornea 4 times daily for 7 d. At concentrations 1000 times the IC50 values, the EB and bHOM peptides showed no toxicity, whereas TAT-C caused some mild eyelid swelling. Some slight epithelial cell sloughing was seen with the bKLA peptide in vivo. These results suggest that these CPPs-and EB in particular-have a favorable toxicity profile, and that further development is warranted.

Animals↗

PubMed1997

Metabolic quantification of lesion volume following experimental traumatic brain injury in the rat.

A reliable and rapid method for quantifying lesion volume following traumatic brain injury (TBI) has vast potential in brain injury research. Staining with 2, 3, 5-triphenyltetrazolium chloride (TTC) provides for demarcation of damaged or infarcted tissue from normal, viable cerebral tissue, in which a red formazan product is formed by reduction during cellular respiration of mitochondrial dehydrogenase enzymes. The present study evaluated the use of TTC staining to quantify the cortical lesion volume in rats undergoing fluid-percussion (FP) brain injury. Male Sprague-Dawley rats (350-450 g, n = 27) were anesthetized (sodium pentobarbital, 60 mg/kg, ip) and subjected to lateral FP brain injury of mild (1.1-1.3 atm, n = 5), moderate (2.0-2.3 atm, n = 9), or high (2.4-2.6 atm, n = 8) severity, while sham (noninjured) animals (n = 5) were anesthetized and surgically prepared without injury. Forty-eight hours after injury animals were sacrificed, brains were stained with TTC, and lesion volumes were calculated. A highly significant correlation was found between cerebral cortical lesion volume (mm3) and severity of brain injury (r = 0.85; p < 0.0001). The mean (+/-SD) lesion volumes were 12.1 (+/-4.5) mm3 following mild injury, 33.8 (+/-8.6) mm3 following moderate injury, and 45.1 (+/-14.0) mm3 following severe injury. A significant difference was observed between all injury groups using a t test with Bonferroni correction (p < 0.05). These results suggest that the TTC staining technique is a useful, rapid, and reproducible method for quantification of lesion volume following lateral FP brain injury.

Animals↗

PubMed1990

Evaluation of quinidine effect on the antitumor activity of adriamycin and mitoxantrone in adriamycin-sensitive and -resistant P388 leukemia cells.

Utilizing the P388 murine leukemia cells sensitive (P388/S) and resistant (P388/ADR) to Adriamycin (ADR), we evaluated the effect of quinidine, an anti-arrhythmic agent, on the cytotoxic activity of ADR and Mitoxantrone (MITO), both in vitro as well as in vivo. Quinidine enhanced the cytotoxicity of both ADR and MITO in P388/S and P388/ADR cells, as assessed by the decrease in color intensity of formazan crystal in the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay. A dose dependent inhibition of 3H-thymidine and 3H-uridine incorporation was observed when the P388/S and P388/ADR cells were exposed to quinidine alone. A non-toxic concentration of quinidine (5 microM) enhanced the DNA biosynthesis inhibition induced by ADR (55 to 65%) and MITO (37 to 44%) in P388/ADR cells, indicating reversal of resistance, while in P388/S cells only a minimal increase in DNA biosynthesis inhibition was observed. The combination of quinidine at doses of 50 to 100 mg/kg significantly potentiated the antitumor activity of ADR and MITO in P388/ADR bearing mice, whereas the potentiation of ADR and MITO antitumor response was lower in P388/S bearing mice. Quinidine increased the cellular levels of ADR by 53 to 126% in P388/ADR cells in vitro, but failed to indicate such elevated levels of cellular ADR in P388/S cells. This enhanced intracellular accumulation of ADR in P388/ADR cells, explains the therapeutic efficacy of ADR and MITO in P388/ADR, both in vitro as well as in vivo. Results suggest the efficacy of quinidine to ameliorate the antitumor effects of ADR and MITO in drug resistant tumor cells.

Animals↗

PubMed1994

Localization of NADPH-diaphorase reactivity in the chick and mouse thyroid gland.

In the present study, nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH-d) histochemistry has been used as a marker for nitric oxide synthase (NOS). The colored reaction product, formazan, was localized in neuronal cell bodies, nerve fibers, and vascular endothelium in the thyroid of chick and mouse. In these two animal species, most of the NADPH-d-labeled neuronal cell bodies were found in the thyroid capsule and interfollicular connective tissue while some were associated with blood vessels. Most nerve fibers travelled with blood vessels supplying the thyroid gland, while a few of them were intimately associated with the thyroid follicular cells. Control sections not incubated with beta-NADPH failed to show labeling of the above structures. It is concluded that nitric oxide may play an important role in endocrine secretion by controlling the regional blood flow in the thyroid gland and by directly acting on the thyroid follicular cells.

Amino Acid Oxidoreductases↗