Abstract
Fumonisin B1 (FB1), belonging to the member of fumonisins, is one of the most toxic mycotoxins produced mainly by Fusarium proliferatum and Fusarium verticillioide. FB1 has caused extensive contamination worldwide, mainly in corn, rice, wheat, and their products, while it also poses a health risk and is toxic to animals and human. It has been shown to cause oxidative stress, endoplasmic reticulum stress, cellular autophagy, and apoptosis. This review focuses on the current stage of FB1 contamination, its toxic effects of acute toxicity, immunotoxicity, organ toxicity, and reproductive toxicity on animals and humans. The potential toxic mechanisms of FB1 are discussed. One of the main aims of the work is to provide a reliable reference strategy for understanding the occurrence and toxicity of FB1.
Highlights
Fumonisins (FUMs) are mycotoxins produced from Fusarium spp
Intravenous and oral administration of fumonisin B1 (FB1) resulted in a significant increase in the Sa/So ratio in the blood and cerebrospinal fluid of pigs, while treatment with fumonisin esterase resulted in a similar Sa/So as in the control group, suggesting that FB1 did interfere with sphingolipid metabolism [52]
Oxidative stress-mediated activation of Jun N-terminal kinase (JNK) simultaneously leads to phosphorylation of B-cell lymphoma-2 (Bcl-2) and release of Beclin1, which indirectly stimulates the expression of LC3- II or LC3- I and induces autophagy [70]
Summary
Fumonisins (FUMs) are mycotoxins produced from Fusarium spp. Among them, the amount of fumonisins produced by Fusarium verticilliodes and Fusarium proliferatum is the most pronounced [1,2]. UTthiosfse4r2i0oufesleydesnwdaenregecrosntthaemhienradtehde,awlthithantdheechoingohmesict dleevveellobpeminegn6t.5I6n8 tμhge/kpget[i2n4d].uTsthriys, sthereiomuasilny ceonmdapnogneernststhoef hsoemrdehpeeatltfhooadnsdaerceocnoormn aicnddewvehleoaptm, seonFt.BI1nctahne aplestoicnodnutsatmryi,ntahtee mpeatinfocoodms.pAolntehnotusgohf istoims neopteatbfuoonddsanatr,eitcoarlsnoacnaduswehs ecahtr,osnoicFBd1amcaangealtsoo pcoetnbtaomdiensa[te25p].et foods It is not abundant, it causes chronic damage to pet bodieTsh[e2e5f]f.ect of FB1 on humans depends mainly on the dietary habits of the area where they Tlihve.efPfeecotpolfeFiBn1aorneahsuwmhaenrsedceoprennadnsdmcaoinrnlypornodthuecdtsieatraeryrehgaubliatsrloyf cthoensauremaewdhaerree ethxepyosleivdet.oPFeoBp1l.eWinheaaretapsrowdhuecrtes,caolrtnhoaungdhcFoBrn pisroadlsuocptsreasreenrtebguutlanrolyt actohnisguhmledvealrse, aerxelpeossehdatromFfBu1l .toWhhueamtapnrso.dIuncttsh, raelethroeumgohteFBT1aniszalnsioanprveislelangt ebsu,tinowt ahtichhigthhelecvheillsd, ’asrefoloesds dhuarimngfuml toonhthusm1a2n–2s.2Iwn athsrpereedreommointeanTtalnyzcaonrinanbavsieldla,g9e6s%, inofwuhriinche stahme cphleilsdt’essftoedodpodsuitrivneg fmoronutrhinsa1r2y–f2u2mwoansispinreBd1o(UmFinBa1n)t[l2y6]c.oKrnigbwaasehda,d96th%e hofiguhreisnteUsFaBm1pgleesomteesteridc mpoesaintiv3e27f.o2r (u2r1i7n.a1r–y49f3u.0m)opngi/simnLB, 1fo(UlloFwB1e)d[b2y6]N. Intravenous and oral administration of FB1 (exposure levels of 139 nmol and 3425 nmol b.w., respectively) resulted in a significant increase in the Sa/So ratio in the blood and cerebrospinal fluid of pigs, while treatment with fumonisin esterase resulted in a similar Sa/So as in the control group, suggesting that FB1 did interfere with sphingolipid metabolism [52]. The ratios of Sa and So are time- and dose-dependent, and can vary depending on the amount of FB1 residing in the organ, which is related to the cell-specific function of sphingolipids in the same organ of different species
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