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Appl Environ Microbiol. 1993 Apr;59(4):981-6. doi: 10.1128/aem.59.4.981-986.1993.
2
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Identification of intermediates in the biosynthesis of PR toxin by Penicillium roqueforti.鉴定罗伊氏乳杆菌生物合成 PR 毒素的中间产物。
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本文引用的文献

1
Isolation and Some Properties of the Enzyme That Transforms Eremofortin C to PR Toxin.异戊烯基转移酶 C 向 PR 毒素转化的酶的分离与性质。
Appl Environ Microbiol. 1985 Jun;49(6):1455-60. doi: 10.1128/aem.49.6.1455-1460.1985.
2
Production of Eremofortins A, B, and C Relative to Formation of PR Toxin by Penicillium roqueforti.青霉属产埃氏菌素 A、B、C 与罗克福青霉产生 PR 毒素的关系。
Appl Environ Microbiol. 1980 Apr;39(4):770-6. doi: 10.1128/aem.39.4.770-776.1980.
3
Acute toxicity of PR toxin, a mycotoxin from Penicillium roqueforti.罗克福青霉产生的霉菌毒素PR毒素的急性毒性
Toxicon. 1982;20(2):433-41. doi: 10.1016/0041-0101(82)90006-x.
4
The effects of Penicillium roqueforti toxin on the activity of rat hepatic DNA polymerases.罗克福青霉毒素对大鼠肝脏DNA聚合酶活性的影响。
Toxicology. 1984 Oct;33(1):43-57. doi: 10.1016/0300-483x(84)90015-5.
5
Biochemical effects of PR toxin on rat liver mitochondrial respiration and oxidative phosphorylation.PR毒素对大鼠肝脏线粒体呼吸和氧化磷酸化的生化作用。
Arch Biochem Biophys. 1984 May 1;230(2):400-11. doi: 10.1016/0003-9861(84)90420-x.
6
Isolation and partial characterization of a mycotoxin from Penicillium roqueforti.从罗克福青霉中分离出一种霉菌毒素并进行部分特性鉴定。
Appl Microbiol. 1973 Jan;25(1):111-4. doi: 10.1128/am.25.1.111-114.1973.
7
Inhibitory effect in vitro of PR toxin, a mycotoxin from Penicillium roqueforti, on the mitochondrial HCO-3-ATPase of the rat brain, heart and kidney.来自罗克福青霉的霉菌毒素PR毒素对大鼠脑、心脏和肾脏线粒体HCO-3-ATP酶的体外抑制作用。
Toxicon. 1986;24(2):153-60. doi: 10.1016/0041-0101(86)90117-0.
8
Factors affecting the production of eremofortin C and PR toxin in Penicillium roqueforti.影响罗克福青霉中埃里莫福汀C和PR毒素产生的因素。
Appl Environ Microbiol. 1991 Sep;57(9):2581-5. doi: 10.1128/aem.57.9.2581-2585.1991.
9
Eremofortin C.A new metabolite obtained from penicillium roqueforti cultures and from biotransformation of PR toxin.岩青霉素C。一种从罗克福青霉培养物以及PR毒素生物转化中获得的新代谢产物。
J Org Chem. 1977 Jul 22;42(15):2632-4. doi: 10.1021/jo00435a023.
10
Inhibition of protein synthesis by PR toxin, a mycotoxin from Penicillium roqueforti.罗克福青霉产生的霉菌毒素PR毒素对蛋白质合成的抑制作用。
FEBS Lett. 1978 Apr 15;88(2):341-4. doi: 10.1016/0014-5793(78)80207-5.

由罗克福青霉降解PR毒素产生的次生代谢产物。

Secondary metabolites resulting from degradation of PR toxin by Penicillium roqueforti.

作者信息

Chang S C, Lu K L, Yeh S F

机构信息

Department of Biochemistry, National Yang-Ming Medical College, Taipei, Taiwan, Republic of China.

出版信息

Appl Environ Microbiol. 1993 Apr;59(4):981-6. doi: 10.1128/aem.59.4.981-986.1993.

DOI:10.1128/aem.59.4.981-986.1993
PMID:8476299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC202226/
Abstract

PR toxin is a secondary metabolite of the fungus Penicillium roqueforti. It is lethal to rats, mice, and cats. Usually, the amount of PR toxin in the culture medium decreases from its maximum on day 15 to zero within 3 to 4 days. We found that two were secondary metabolites produced in the culture medium of this fungus while the production of PR toxin was decreasing. We isolated and purified the two compounds in pure and colorless crystalline form. On the basis of elemental analysis and mass, 1H and 13C nuclear magnetic resonance, infrared, and UV spectroscopies, the two compounds were identified as PR-imine (C17H21O5N) and PR-amide (C17H21O6N). The structures of both compounds and of PR toxin (C17H20O6) were closely related, and the peak production of PR toxin appeared earlier than those of PR-imine and PR-amide. Moreover, PR toxin was transformed to PR-imine when PR toxin was incubated with the culture medium on a given culture day. Thus, we propose that PR toxin is degraded into PR-imine and PR-amide in the culture medium of P. roqueforti.

摘要

PR毒素是罗克福青霉产生的一种次级代谢产物。它对大鼠、小鼠和猫具有致死性。通常，培养基中PR毒素的含量从第15天的最大值在3至4天内降至零。我们发现，在这种真菌的培养基中，当PR毒素的产量下降时，会产生两种次级代谢产物。我们以纯净无色晶体形式分离并纯化了这两种化合物。基于元素分析、质谱、1H和13C核磁共振、红外和紫外光谱，这两种化合物被鉴定为PR-亚胺（C17H21O5N）和PR-酰胺（C17H21O6N）。这两种化合物以及PR毒素（C17H20O6）的结构密切相关，PR毒素的产量峰值比PR-亚胺和PR-酰胺出现得更早。此外，在特定培养日将PR毒素与培养基一起孵育时，PR毒素会转化为PR-亚胺。因此，我们提出PR毒素在罗克福青霉的培养基中会降解为PR-亚胺和PR-酰胺。