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A sensitive and rapid method had been developed for the simultaneous determination of ochratoxin A (OTA)and zearalenone (ZEN)in corn, wheat and rice by high performance liquid chromatography (HPLC). After extraction with acetonitrile and water (80/20, volume ratio)for 30 min under 30 °C and 200 r/min in a rotary shaker, the cereal samples were purified using Oasis PRiME HLB cartridge. The limits of detection and quantification of the mycotoxins were determined under the optimum HPLC conditions at 3.7 µg/kg and 12.25 µg/kg for ZEN and 0.11 µg/kg and 0.38 µg/kg for OTA, respectively. High correlation coefficients (R² > 0.99) were obtained in the range of 10 µg/kg-2 000 µg/kg for ZEN and 0.2 µg/kg-200 µg/kg for OTA. The average recoveries ranged from 83.0 % to 101.3 % for different concentrations of ZEN and OTA in spiked samples along with good intra-day (3.12 %-7.03 %)and inter-day (3.57 %-9.3 %)precision. The method proposed is suitable for the simultaneous determination of ZEN and OTA and can be performed for the mycotoxin analysis in corn, wheat and rice. [ABSTRACT FROM AUTHOR]

Neuronal apoptosis is crucial in neurodegenerative diseases. However, a lower apoptotic rate of nerve cells is detected in the brain compared to that in other organs in neurodegenerative patients or in animal models, suggesting that neuronal apoptosis induced by any type of risk factors is intricately regulated. Human and animal studies demonstrated that a high concentration of oxidized LDL (ox-LDL) in the brain, which is associated with hyperlipidemia, is one of the key apoptosis inducers in neurodegenerative diseases. However, the mechanism underlying the ox-LDL-mediated regulation of neuronal apoptosis has not been fully elucidated. Recently, we investigated proprotein convertase subtilisin/kexin type 9 (PCSK9), a striking gene involved in lipid metabolism that exhibits a positive correlation with macrophage and endothelial cell apoptosis induced by ox-LDL. Moreover, PCSK9 may degrade β-site amyloid precursor protein-cleaving enzyme 1 (BACE1), the key enzyme cleaving amyloid precursor protein (APP) to generate amyloid β peptide (Aβ). Aβ is another key apoptosis inducer in neurodegenerative diseases. Our findings indicated that PCSK9 may be upregulated by the high levels of ox-LDL in the brain associated with hyperlipidemia and promote neuronal apoptosis through the NF-κB-B-cell lymphoma 2 (Bcl-2)/Bax-caspase 9-caspase 3 signaling pathways. Moreover, increased PCSK9 levels may inhibit the APP/Aβ metabolic pathway and reduce Aβ generation by degrading BACE1, thereby decreasing Aβ-induced neuronal apoptosis. The dual regulation mechanism of PCSK9 on apoptosis maintains neuronal apoptosis induced by risk factors at low levels.