Glucose handling in streptozotocin-induced diabetic rats is improved by tyramine but not by the amine oxidase inhibitor semicarbazide

Diabetes mellitus (DM) constitutes one of the public health problems today. It is characterized by hyperglycemia through a defect in the β-cells function and/or decreased insulin sensitivity. Apocynin has been tasted acting directly as an NADPH oxidase inhibitor and reactive oxygen species (ROS) scavenger, exhibiting beneficial effects against diabetic complications. Hence, the present study’s goal was to dissect the possible mechanisms by which apocynin could mediate its cardioprotective effect against DM-induced oxidative stress. Male Wistar rats were assigned into 4 groups: Control (C), control + apocynin (C+A), diabetes (D), diabetes + apocynin (D+A). DM was induced with streptozotocin. Apocynin treatment (3 mg/kg/day) was applied for 5 weeks. Treatment significantly decreased blood glucose levels and insulin resistance in diabetic rats. In cardiac tissue, ROS levels were higher, and catalase enzyme activity was reduced in the D group compared to the C group; the apocynin treatment significantly attenuated these responses. In heart mitochondria, Complexes I and II of the electron transport chain (ETC) were significantly enhanced in the D+A group. Total glutathione, the level of reduced glutathione (GSH) and the GSH/ oxidized glutathione (GSSG) ratio were increased in the D+A group. Superoxide dismutase (SOD) and the glutathione peroxidase (GSH-Px) activities were without change. Apocynin enhances glucose uptake and insulin sensitivity, preserving the antioxidant defense and mitochondrial function.

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Diabetes induces pulmonary artery endothelial dysfunction by NADPH oxidase induction

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.90354.2008 ◽

2008 ◽

Vol 295 (5) ◽

pp. L727-L732 ◽

Cited By ~ 43

Author(s):

Jose G. Lopez-Lopez ◽

Javier Moral-Sanz ◽

Giovanna Frazziano ◽

Maria J. Gomez-Villalobos ◽

Jorge Flores-Hernandez ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Nadph Oxidase ◽

Pulmonary Arteries ◽

Diabetic Rats ◽

Oxidase Inhibitor ◽

No Synthase ◽

Superoxide Production ◽

Regulatory Subunit ◽

Sprague Dawley ◽

Relaxant Response

Recent data suggest that diabetes is a risk factor for pulmonary hypertension. The aim of the present study was to analyze whether diabetes induces endothelial dysfunction in pulmonary arteries and the mechanisms involved. Male Sprague-Dawley rats were randomly divided into a control (saline) and a diabetic group (70 mg/kg−1 streptozotocin). After 6 wk, intrapulmonary arteries were mounted for isometric tension recording, and endothelial function was tested by the relaxant response to acetylcholine. Protein expression and localization were measured by Western blot and immunohistochemistry and superoxide production by dihydroethidium staining. Pulmonary arteries from diabetic rats showed impaired relaxant response to acetylcholine and reduced vasoconstrictor response to the nitric oxide (NO) synthase inhibitor l-NAME, whereas the response to nitroprusside and the expression of endothelial NO synthase remained unchanged. Endothelial dysfunction was reversed by addition of superoxide dismutase or the NADPH oxidase inhibitor apocynin. An increase in superoxide production and increased expression of the NADPH oxidase regulatory subunit p47phox were also found in pulmonary arteries from diabetic rats. In conclusion, the pulmonary circulation is a target for diabetes-induced endothelial dysfunction via enhanced NADPH oxidase-derived superoxide production.

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EFFECT OF AN AMINE-OXIDASE INHIBITOR ON ARTERIAL AMMONIUM LEVELS IN LIVER DISEASE

The Lancet ◽

10.1016/s0140-6736(57)91849-4 ◽

1957 ◽

Vol 269 (6983) ◽

pp. 1332-1333 ◽

Cited By ~ 10

Author(s):

A.M. Dawson ◽

Sheila Sherlock

Keyword(s):

Liver Disease ◽

Amine Oxidase ◽

Oxidase Inhibitor

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THERAPEUTIC RE-ORIENTATION IN SOME DEPRESSIVE STATES: CLINICAL EVALUATION OF A NEW MONO-AMINE OXIDASE INHIBITOR (W-1544-A) (PHENELZINE (NARDIL)

American Journal of Psychiatry ◽

10.1176/ajp.116.5.429 ◽

1959 ◽

Vol 116 (5) ◽

pp. 429-434 ◽

Cited By ~ 11

Author(s):

WILLIAM FURST

Keyword(s):

Clinical Evaluation ◽

Amine Oxidase ◽

Oxidase Inhibitor ◽

Depressive States

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THE EFFECT OF 5-HYDROXYTRYPTAMINE AND OF AN AMINE OXIDASE INHIBITOR ON EXPERIMENTAL DECIDUOMATA IN MICE

Journal of Endocrinology ◽

10.1677/joe.0.0230209 ◽

1961 ◽

Vol 23 (2) ◽

pp. 209-215 ◽

Cited By ~ 8

Author(s):

D. LINDSAY ◽

E. POULSON ◽

J. M. ROBSON

Keyword(s):

Monoamine Oxidase ◽

Toxic Effect ◽

Corpus Luteum ◽

Amine Oxidase ◽

Oxidase Inhibitor ◽

Toxic Effects ◽

Endocrine Activity ◽

Direct Toxic Effect ◽

Decidual Tissue ◽

Decidual Reaction

SUMMARY Investigations were carried out to study the mechanism by which 5-hydroxytryptamine (5-HT) and monoamine oxidase inhibitors interfere with pregnancy, using the experimental decidual reaction in mice. The results suggest that both 5-HT and an amine oxidase inhibitor, HP. 1325 (2,2′-(p-phenylenedioxy)-di-(ethyl hydrazinium (1+) chloride)), interfere with the endocrine activity of the ovary, particularly the corpus luteum, since their toxic effects on deciduomata are reversed by progesterone. In addition, 5-HT also has a direct toxic effect on decidual tissue.

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