This page lists medical journal articles discussing the association between other health issues and the mycotoxin known as penitrem A.
The Health Effects of Penitrem A page of the Paradigm Change site provides further information on the effects of this mycotoxin.
Song B., Marvizón J. C.. N-methyl-D-aspartate receptors and large conductance calcium-sensitive potassium channels inhibit the release of opioid peptides that induce mu-opioid receptor internalization in the rat spinal cord. Neuroscience. 2005;136:549– 562. PMID: 16203108
Endogenous opioids in the spinal cord play an important role in nociception, but the mechanisms that control their release are poorly understood. mu-Opioid receptor internalization evoked by high K+ or veratridine was also inhibited by N-methyl-D-aspartate receptor activation.We hypothesized that this inhibition was mediated by large conductance Ca2+-sensitive K+ channels BK(Ca2+). Indeed, inhibition by N-methyl-D-aspartate was prevented by tetraethylammonium and by the selective BK(Ca2+) blockers paxilline, penitrem A and verruculogen.
Vigh Jozsef, Solessio Eduardo, Morgans Catherine W., Lasater Eric M.. Ionic mechanisms mediating oscillatory membrane potentials in wide-field retinal amacrine cells. Journal of neurophysiology. 2003;90:431–443. PMID: 12649310
Particular types of amacrine cells of the vertebrate retina show oscillatory membrane potentials (OMPs) in response to light stimulation. Here we characterized the ionic mechanisms responsible for the oscillations in wide-field amacrine cells (WFACs) in an effort to better understand the functional properties of the cell. The OMPs were found to be calcium (Ca2+) dependent; blocking voltage-gated Ca2+ channels eliminated the oscillations, whereas elevating extracellular Ca2+ enhanced them. The initiation of OMPs depended on penitrem-A-sensitive (BK) K(Ca) channels, whereas their duration is under apamin-sensitive (SK) K(Ca) channel control.
Sabater-Vilar Monica, Nijmeijer Sandra, Fink-Gremmels Johanna. Genotoxicity assessment of five tremorgenic mycotoxins (fumitremorgen B, paxilline, penitrem A, verruculogen, and verrucosidin) produced by molds isolated from fermented meats. Journal of food protection. 2003;66:2123–2129. PMID: 14627292
Tremorgenic mycotoxins are a group of fungal metabolites known to act on the central nervous system, causing sustained tremors, convulsions, and death in animals. We assessed the genotoxicity of five tremorgenic mycotoxins (fumitremorgen B, paxilline, penitrem A, verrucosidin, and verruculogen) associated with molds found in fermented meats. According to the results obtained in this study, all of the investigated mycotoxins except penitrem A exhibited a certain degree of genotoxicity.
Wadsworth S. J., Chander A.. H+-and K+-dependence of Ca2+ uptake in lung lamellar bodies. The Journal of membrane biology. 2000;174:41–51. PMID: 10741431
In this study, we investigated the Ca2+ uptake characteristics in isolated lung lamellar bodies. The inhibitors of Ca2+-activated K+-channels, tetraethylammonium, Penitrem A, and 4-aminopyridine, also inhibited the K+-dependent Ca2+ uptake at 700 nM Ca2+. Thus the uptake of Ca2+ in isolated lung lamellar bodies appears to be regulated by two mechanisms, (i) the H+-gradient and (ii) the K+ transport across the lamellar body membrane. We speculate that lamellar bodies accumulate Ca2+ and contribute to regulation of cytosolic Ca2+ in type II cells under resting and stimulated conditions.
Adeagbo A. S.. 1-Ethyl-2-benzimidazolinone stimulates endothelial K(Ca) channels and nitric oxide formation in rat mesenteric vessels. European journal of pharmacology. 1999;379:151–159. PMID: 10497901
Hyperpolarization of most blood vessels occurs by the opening of K(Ca) channels. 1-Ethyl-2-benzimidazolinone (1-EBIO) is a direct activator of K(Ca) channels in epithelial cells and is potentially valuable for studying cellular hyperpolarization. This study reports the effects of 1-EBIO on isolated rat mesenteric beds perfused with normal (4.7 mM), or high (20 or 80 mM) K+ physiological salt solution (PSS) and constricted with an alpha1-adrenoceptor agonist, cirazoline (0.3-1 microM). Infusion of penitrem A (100 nM), a maxi-K+ channel blocker, or apamin (0.5 microM), a small-conductance (SK(Ca)) K+ channel blocker, produced significant increases in cirazoline-mediated tone. 1-EBIO relaxations were attenuated by penitrem A.
Berman R. S., Griffith T. M.. Spatial heterogeneity in the mechanisms contributing to acetylcholine-induced dilatation in the rabbit isolated ear. British journal of pharmacology. 1998;124:1245–1253. PMID: 9720797
Using an X-ray microangiographic technique in rabbit isolated perfused ears preconstricted with 5-HT (300 nM) and histamine (300 nM), we investigated the combined actions of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin on acetylcholine-induced depressor responses. In the presence of L-NAME (300 microM) and indomethacin (10 microM), this depressor action was reduced. Two calcium-activated K+ channels blockers, charybdotoxin (ChTX; 10 nM) and penitrem A (100 nM), further inhibited, but did not abolish, the L-NAME- and indomethacin-resistant response to acetylcholine (10 nM-300 microM). Both agents abolished the vasodilatory action of acetylcholine in G2. 5. The L-NAME- and indomethacin-resistant component was inhibited by ChTX and penitrem A, suggesting it is mediated, at least in part, by activation of K(Ca) channels and could therefore involve a hyperpolarising mediator such as endothelium-derived hyperpolarising factor.
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