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Fumonisin B1: a neurotoxic mycotoxin (CROSBI ID 197971)

Prilog u časopisu | pregledni rad (znanstveni) | međunarodna recenzija

Domijan, Ana-Marija Fumonisin B1: a neurotoxic mycotoxin // Arhiv za higijenu rada i toksikologiju, 63 (2012), 4; 531-544. doi: 10.2478/10004-1254-63-2012-2239

Podaci o odgovornosti

Domijan, Ana-Marija

engleski

Fumonisin B1: a neurotoxic mycotoxin

Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium spp. moulds that contaminate crop, predominantly maize, all around the world. More than 15 types of fumonisins have been indentified so far, but FB1 is the most abundant and toxicologically the most significant one. FB1 has a wide range of toxic effects, depending on animal species. In horses FB1 causes equine leukoencephalomalacia (ELEM), in pigs pulmonary oedema and in experimental rodents nephrotoxicity and hepatotoxicity. In humans exposure to FB1 is linked with higher incidence of primary liver cancer and oesophageal cancer, which are frequent in certain regions of the world (such as Transkei region in South Africa) where maize is staple food. The occurrence of neural tube defect in children in some countries of Central America (such as Mexico and Honduras) is connected with the consumption of FB1-contaminated maize-based food. However, possible involvement of FB1 in the development of human diseases is not clear. Nevertheless, the International Agency for Research on Cancer (IARC) has classified FB1 as a possible carcinogen to humans (group 2B). FB1 is a causative agent of ELEM, a brain disorder in equines, indicating that brain is a target organ of FB1 toxicity. Several studies on experimental animals or on cell cultures of neural origin have established that FB1 has a neurodegenerative potential, although the mechanism of its neurotoxicity is still vague. The aim of this article is to give an overview of available literature on FB1 neurotoxicity and involved mechanisms, and to offer a new perspective for future studies.

equine leukoencephalomalacia; neural tube defect; neurotransmitters; sphingolipids; sphingoid bases; oxidative stress; mitochondria

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Podaci o izdanju

63 (4)

2012.

531-544

objavljeno

0004-1254

10.2478/10004-1254-63-2012-2239

Povezanost rada

Javno zdravstvo i zdravstvena zaštita, Farmacija

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