Biotin analogs activate guanylate cyclase

Vesely, David L.; Wormser, Henry C.; Abramson, H. N.

doi:10.1007/bf00222480

Cited by 16 publications

(8 citation statements)

References 17 publications

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“…Previous studies provide convincing evidence that biotin and its metabolite biotinyl-AMP activate soluble guanylate cyclase, increasing the synthesis of cGMP (22, 40, 41). Subsequently, cGMP activates PKG, thereby increasing the transcription of genes coding for biotin-dependent carboxylases and holocarboxylase synthetase (22).…”

Section: Discussionmentioning

confidence: 98%

Nitric Oxide Signaling Depends on Biotin in Jurkat Human Lymphoma Cells

Rodriguez-Melendez

Zempleni

2009

The Journal of Nutrition

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Biotin affects gene expression through a diverse array of cell signaling pathways. Previous studies provided evidence that cGMP-dependent signaling also depends on biotin, but the mechanistic sequence of cGMP regulation by biotin is unknown. Here we tested the hypothesis that the effects of biotin in cGMP-dependent cell signaling are mediated by nitric oxide (NO). Human lymphoid (Jurkat) cells were cultured in media containing deficient (0.025 nmol/L), physiological (0.25 nmol/L), and pharmacological (10 nmol/L) concentrations of biotin for 5 wk. Both levels of intracellular biotin and NO exhibited a dose-dependent relationship in regard to biotin concentrations in culture media. Effects of biotin on NO levels were disrupted by the NO synthase (NOS) inhibitor N-monomethyl-arginine. Biotin-dependent production of NO was linked with biotin-dependent expression of endothelial and neuronal NOS, but not inducible NOS. Previous studies revealed that NO is an activator of guanylate cyclase. Consistent with these previous observations, biotin-dependent generation of NO increased the abundance of cGMP in Jurkat cells. Finally, the biotin-dependent generation of cGMP increased protein kinase G activity. Collectively this study is consistent with the hypothesis that biotin-dependent cGMP signaling in human lymphoid cells is mediated by NO.

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Section: Discussionmentioning

confidence: 98%

Nitric Oxide Signaling Depends on Biotin in Jurkat Human Lymphoma Cells

Rodriguez-Melendez

Zempleni

2009

The Journal of Nutrition

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“…Thus, the effects attributed to B complex vitamins can be reproduced by this intracellular messenger by itself. In a recent investigation using biotin analogues, only those with biological activity were able to enhance guanylate cyclase activity [13]. The analogues without biological activity did not enhance guanylate cyclase activity [13].…”

Section: Discussionmentioning

confidence: 99%

“…Without the guanylate cyclase cofactor manganese present, biotin is unable to maximally stimulate guanylate cyclase activity [13]. A series of experiments were done to determine whether the concentration of the guanylate cyclase cofactor manganese affected any of the B complex vitamins' activation of hepatic guanylate cyclase.…”

Section: Interrelationship Of the Guanylate Cyclase Cofactor Manganesmentioning

confidence: 99%

B complex vitamins activate rat guanylate cyclase and increase cyclic GMP levels

Vesely

1985

Eur J Clin Investigation

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Since B complex vitamins and the intracellular messenger cyclic guanosine monophosphate (GMP) have similar effects of promoting growth, DNA and protein synthesis, the present investigation was designed to determine if the B complex vitamins' mechanism of action might involve cyclic GMP. All of the B complex vitamins increased rat cyclic GMP tissue levels. The cause of these increased cyclic GMP levels was activation of the enzyme guanylate cyclase [E.C.4.6.1.2.] which was increased significantly (P less than 0.001) in a variety of tissues at the l nmol l-1 concentration of these vitamins. The maximal activation of this enzyme required the presence of manganese ion. The present investigation suggests that the guanylate cyclase-cyclic GMP system may play a role in the mechanism of action of B complex vitamins at the cellular level.

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“…Previous studies have shown that pyridoxine including the other B complex vitamins promote their effects by activating GC via enhancing cGMP levels [17,28].…”

Section: Discussionmentioning

confidence: 99%

The Role of L-Arginine/Nitric Oxide Pathway in the Antinociceptive Activity of Pyridoxine in Mouse

Abacıoğlu

Tunçtan

Çakıcı

et al. 2011

Arzneimittelforschung

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In the present study the role of L-arginine/nitric oxide (NO)/cGMP pathway in the antinociceptive activity of pyridoxine in p-benzoquinone-induced abdominal constriction test in mouse was investigated. Pyridoxine (CAS 58-56-0) displayed dose-dependent antinociceptive activity at 0.0625−1 mg/kg (s.c.) doses. L-arginine (CAS 1119-34-2), a NO precursor, displayed a triphasic pattern as antinociception-nociceptionantinociception (61.8 ± 7.8, −36.5 ± 12.7 and 17.0 ± 4.3 %, 5, 40 and 50 mg/kg, s.c., respectively). The antinociceptive effect of pyridoxine at ED 50 dose (0.43 mg/ kg, s.c.) (47.7 ± 3.9 %) was significantly decreased by L-arginine at 40 and 50 mg/ kg doses (4.1 ± 9.3 and 37.8 ± 1.6 %, respectively) while 5 mg/kg dose of L-arginine significantly potentiated the pyridoxine analgesia. On the other hand, pyridoxine reversed the L-arginine-induced nociception to antinociception (4.1 ± 9.3 %) and augmented the antinociceptive effect of L-arginine (37.8 ± ZusammenfassungDie Rolle von L-Arginin/Stickoxid in der antinozizeptiven Aktivität von Pyridoxin bei Mäusen Ziel dieser Studie war es, die Rolle von L-Arginin/Stickoxid (NO)/cGMP in der antinozizeptiven Aktivität von Pyridoxin im p-Benzochinon.induzierten abdominal Spannungstest zu untersuchen. Pyridoxin (CAS 58-56-0) zeigte eine dosisab-1.6 %). L-N G -nitroarginine methyl ester (CAS 51298-62-5), a NO synthase inhibitor, at 75 mg/kg, s.c. produced antinociception and significantly increased the antinociceptive effect of pyridoxine (63.7 ± 1.2 %). Methylene blue (CAS 61-73-4, MB), a guanylyl cyclase and/or NO synthase inhibitor, was antinociceptive and nociceptive at 5 and 40 mg/kg doses, respectively. 5 mg/kg dose of MB significantly increased the antinociceptive effect of pyridoxine, but did not change it at 40 mg/kg dose. On the other hand, pyridoxine significantly decreased the antinociceptive effect of MB and reversed the MB-induced nociception to antinociception. Combination of pyridoxine and morphine (CAS 57-27-2) (ED 50 : 0.13 mg/kg, s.c.) at 49.8 ± 1.9 % revealed a significant antinociceptive potentiation (69.1 ± 1.8 %). The findings of the present study emphasise the contribution of central and/or peripheral L-arginine/NO/ cGMP nociceptive processes in pyridoxine-induced antinociception. hängige antinozizeptive Aktivität in einer subkutanen Dosis von 0,0625-1 mg/kg. L-Arginin (CAS 1119-34-2), ein NO-Precursor, zeigte ein Drei-Phasen-Muster: Antinozizeption-NozizeptionAntinozizeption ( 61.8 ± 7.8, 36.5 ± 12.7 bzw. 17.0 ± 4.3 %, 5, 40 bzw. 50 mg/kg, s.c.). Der antinozizeptive Effekt von Pyridoxin bei Verwendung der ED 50 (0.43 mg/kg, s.c.) (47.7 ± 3.9) wurde von L-ArgiKey words L-Arginine/NO/cGMP, role in antinociception CAS 58-56-0 CAS 1119-34-2 Pyridoxine, antinociceptive effect, mouse Arzneim.-Forsch./Drug Res. 51 (II), 832−838 (2001) Arzneim.-Forsch./Drug Res. 51 (II), 832−838 (2001) 832 Abacıoglu, et al. − L-Arginine/nitric oxide pathway

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Biotin analogs activate guanylate cyclase

Cited by 16 publications

References 17 publications

Nitric Oxide Signaling Depends on Biotin in Jurkat Human Lymphoma Cells

Nitric Oxide Signaling Depends on Biotin in Jurkat Human Lymphoma Cells

B complex vitamins activate rat guanylate cyclase and increase cyclic GMP levels

The Role of L-Arginine/Nitric Oxide Pathway in the Antinociceptive Activity of Pyridoxine in Mouse

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