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Fumonisin B1: A Potential Risk Factor for Neural Tube Defects

Domijan, Ana-Marija; Šegvić Klarić, Maja; Žanić-Grubišić, Tihana; Rumora, Lada
Fumonisin B1: A Potential Risk Factor for Neural Tube Defects // Fumonisins: Natural Occurrence, Management Practices and Health Concerns / Evans, Craig M. (ur.).
New York: Nova Science Publishers, 2015. str. 27-40

Fumonisin B1: A Potential Risk Factor for Neural Tube Defects

Domijan, Ana-Marija ; Šegvić Klarić, Maja ; Žanić-Grubišić, Tihana ; Rumora, Lada

Vrsta, podvrsta i kategorija rada
Poglavlja u knjigama, znanstveni

Fumonisins: Natural Occurrence, Management Practices and Health Concerns

Evans, Craig M.

Nova Science Publishers

New York


Raspon stranica


Ključne riječi
Fumonisin B1, mycotoxin, neural tube defects, sphinganine, sphingosine, sphingolipids, folic acid

Fumonisin B1 (FB1) is a mycotoxin and a secondary product of Fusarium spp. molds. The predominant producer of FB1 is F. verticillioides (formerly known as F. moniliforme). Fusarium spp. molds and FB1 are common contaminants of maize worldwide. The toxicity of FB1 was first observed in farm animals ; in horses, exposure to FB1-contaminated feed has been associated with equine leukoencephalomalacia, and in pigs with pulmonary edema. For experimental animals, FB1 is hepatotoxic, nephrotoxic and carcinogenic. In some regions of the world where maize is a staple food, increased incidences of human esophageal and liver cancers as well as increased frequency of neural tube defects (NTDs) have been observed and related to FB1 exposure. NTDs are congenital malformations that occur as a result of failure of neural tube closure during early embryogenesis ; in humans, the most common NTDs are anencephaly and spina bifida. Several lines of evidence point to an association between FB1 and development of NTDs. It has been well-established that FB1, due to its structural similarities with sphingoid bases sphinganine and sphingosine, alters sphingolipid metabolism. That in turn affects cell signal transduction pathways and folate receptor functioning. Therefore, FB1-provoked impairment of sphingolipid metabolism has been suggested as a possible mechanism by which FB1 induces the development of NTDs. Experimental studies have confirmed the embryotoxicty and teratogenicity of FB1. Epidemiological studies demonstrated that maternal exposure to FB1 (through consumption of FB1-contaminated maize-based food) could be implicated in higher NTD occurrences. In this review, data associating exposure to FB1 with the development of NTDs are presented.

Izvorni jezik

Znanstvena područja
Javno zdravstvo i zdravstvena zaštita, Farmacija


Farmaceutsko-biokemijski fakultet, Zagreb