Research On Contamination And Toxicology Of Zearalenone In Paddy Rice

Zearalenone (ZEA) was first called as the F-2toxin, it’s a class ofnon-steroidal estrogen produced mainly by Fusarium, can cause paddy ricepollution all over the word. It attracted wordwide attention while it lead to variousdiseases to human and animals, and lead to economic losses.The article analyzed the contamination of Zearalenone in paddy rice in theseven provinces of China, and compared its distribution regulation. As thecontaminated rice often used as feed, we continue to explore the toxicokinetics ofZEA in piglet, established the kinetic equation of ZEA and its main metabolites.Based on the existing toxicity, we further studied the cytotocity of ZEA and itsmain metabolites α-ZOL and β-ZOL. After in vitro study we continued to exploredthe mechanism of oxidative damage of ZEA in vivo, flavone was chosen asantioxidants to validate the oxidative damage. The main results were as follows:(1) The contamination of ZEA was very common in our country, and hassignificant difference in different areas; the detection rate and exceeded rate were25.4%and9.52%. The most serious pollut province is Fujian, the contaminationalso significantly effected by harvest season.(2) Five weaned piglet (Duroc×Large White×Landrace)), which were50±2days old and weight10±2kg, one-time neck intramuscular injection with the doseof2mg/kg b.w., collect neck vein blood, HPLC detects and the data were analyzedwith pharmacokinetics computer program3P97. Results showed that: ZEA ismainly metabolism for α-ZOL, the metabolic model of ZEA and α-ZOL could bedescribed as one-compartment model with1storder absorption in blood, and themetabolism equation were C=0.113e-0.473tand C=0.050e-0.297t. ZEA and α-ZOL wereeliminated very quickly as they could eliminate47%and30%of the residues; theywere mainly distributed in cells, uptaked by tissue and organs, with lowconcentration in extracellular. The main pharmacokinetics parameters in bloodwere: CL8.35、11.97L kg-1h-1; t1/2β1.46、2.33h; AUC0.239、0.167mg L-1h-1; V/f17.64、40.33L kg-1; Ke0.47、0.30h-1.(3) People liver cell L02and the original embryo kidney people transformedcell lines (293Ad5+) were used to detect the cytotoxity of ZEA and its metabolites.The IC50of ZEA, α-ZOLand β-ZOL to293cell were31、26、40μg/ml, the cytotoxitywere α-ZOL＞ZEA＞β-ZOL. The IC50of ZEA, α-ZOLand β-ZOL to L02cell were48、56、90μg/ml, the cytotoxity were ZEA＞α-ZOL＞β-ZOL. It’s also showed thatthe β-ZOL has low cytotoxity while it’s only in high concentration caused significance inhibition.(4) Seventy mice (10mice/group with male and female each half) were dividedinto seven groups as follows: olive oil control groups; ZEA treated groups (10,20,40mg/kg b.w.);24h flavone pre-treated groups (28,56,112mg/kg b.w.) beforetreated with ZEA (40mg/kg b.w.). The induction of oxidative damage in serum andliver was determined by GSH-PX, T-AOC, SOD and MDA levels. Results showedthat ZEA significantly decreased GSH-PX、 SOD、 and T-AOC levels whilesignificantly increased MDA level both in serum and liver. ZEA treatmentcombined with the three doses of flavone showed a total reduction of ZEA inducedoxidative damage. This finding suggested that ZEA may attenuate antioxidantdefense in Kunming mice and pre-treatment with flavone is effective in theprotection against ZEA hazards.