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Pyrrolizidine alkaloids (PAs) are a class of natural toxins produced by plant secondary metabolism, of which unsaturated PAs and most pyrrolizidine alkaloid N-oxides (PANOs) have multiple toxic effects. These toxic components can be transmitted through food supplements or food chain to threaten human health. To date, PAs have been found to be widely present in a variety of food and agricultural products such as honey and tea, highlighting their occurrence as a concerning food safety issue. Therefore, this paper summarizes the contamination levels and possible contamination pathways of PAs in different matrices of different countries, and reviews the latest advances and development trends in pretreatment methods and analytical detection techniques or cooking preparation on the stability of PAs contaminants, aiming to provide warning and reference basis for the detection research, safety risk assessment and control of PAs in foods.

Alkaloids are a large class of secondary metabolites in plants with significant pharmacological activity. As the active ingredients of many Chinese herbal medicines, they have great application value in clinical medicine. However, most alkaloids have obvious toxic effects and can be transmitted into the human body through the food chain, becoming an emerging potential risk factor for public health. This article reviews the types, sources and analytical methods of high-risk toxic and harmful alkaloids in food, aiming to provide warnings and reference for the detection and research of toxic and harmful alkaloids and the policy formulation of relevant regulatory authorities.

In order to establish a fast detection method for the living Zygosaccharomyces rouxii (Z. rouxii) cells in honey and honey products, the performance of propidium monoazide bromide (PMA) and enhanced propidium monoazide bromide (PMAXX) combined with real-time PCR for detecting living cells of Z. rouxii was compared. PMAXX was chosen as the added agent because of its better performance. The optimal concentration of PMAXX was found to be 76.92 μM in cell solution (the cell concentration was 1.0 × 108 CFU/mL). The LODs of PMAXX-qPCR in detecting Z. rouxii in pure MEA and honey solution were found to be 103 and 101 CFU/mL, respectively. Living Z. rouxii cells in 18 real honey samples were detected using this PMAXX-qPCR method and compared with the plate count method. The two methods showed consistent detection results in ten negative samples. In the other eight plate count zero but PMAXX-qPCR-positive samples, further verification experiments showed that six of the PMAXX-qPCR-positive samples contained viable but nonculturable (VBNC) Z. rouxii, while the other two PMAXX-qPCR-positive samples may have contained DNA contamination of Z. rouxii. This method is not only fast and sensitive but also can detect both culturable and viable but nonculturable Z. rouxii. This study provides a promising fast and culture-independent method for the detection of living Z. rouxii cells in honey and honey products.

Meat adulteration is currently a common practice worldwide. In China, adulteration of donkey meat products with the similar species (horse and mule/hinny) meat and mislabeling are becoming widespread concerns. In this study, a sensitive and species-specific duplex real-time PCR assay based on the simultaneous amplification of fragments of the creatine kinase muscle gene family, was developed and optimized for the identification of horse, donkey and mule /hinny species in raw and heat-processed meat products. Duplex real-time PCR results showed different fluorescence amplification curves for horse and donkey. Both kinds of fluorescence amplification curves appeared simultaneously for mule/hinny. The limit of detection (LOD) of the method was up to 0.01 ng /μL. The method and strategy developed in this study could be applied to detect the presence of adulterants from horse and mule /hinny meat in raw donkey meat and meat products.

Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.

Background: The beta 3-adrenoceptor (β3-AR) is closely associated with energy metabolism. This study aimed to explore the role of β3-AR in energy remodeling in a rabbit model of pacing-induced atrial fibrillation (AF). Methods: Rabbits with a sham-operation or pacing-induced AF were used for this study, and the latter group was further divided into three subgroups: 1) the pacing group, 2) the β3-AR agonist (BRL37344)-treated group, and 3) the β3-AR antagonist (SR59230A)-treated group. Atrial electrogram morphology and surface ECG were used to monitor the induction of AF and atrial effective refractory period (AERP). RT-PCR and western blot (WB) were used to show alterations in β3-AR and metabolic-related protein. Results: RT-PCR and WB results showed that β3-AR was significantly upregulated in the pacing group, and that it corresponded with high AF inducibility and significantly decreased AERP200 and ATP production in this group. Inhibition of β3-AR decreased the AF induction rate, reversed AERP200 reduction, and restored ATP levels in the AF rabbits. Further activation of β3-AR using agonist BRL37344 exacerbated AF-induced metabolic disruption. Periodic acid Schiff (PAS) and Oil Red O staining showed β3-AR-dependent glycogen and lipid droplet accumulation in cardiac myocytes with AF. Glucose transporter-4 (GLUT-4) and CD36, key transporters of glucose and fatty acids, were downregulated in the pacing group. Expression of carnitine-palmitoyltransferase I (CPT-1), a key regulator in fatty acid metabolism, was also significantly downregulated in the pacing group. Reduced glucose transportation and fatty acid oxidation could be restored by inhibition of β3-AR. Furthermore, key regulators of metabolism, peroxisome proliferator-activated receptor-α (PPARα) and PPAR co-activator (PGC-1α) can be regulated by pharmacological intervention of the β3-AR. Conclusions: β3-AR is involved in metabolic protein remodeling in AF. PPARα/PGC-1α signaling pathway might be the relevant down-stream molecular machinery in response to AF-induced activation of β3-AR. β3-AR might be a novel target in AF treatment.

ABSTRACT Biosensor detecting techniques have attracted much attention in the content determination of H2O2, which has been used illegally as a food additive. An electrochemical biosensing membrane for the detection of H2O2 was developed with C6-OH of chitosan immobilized cyclodextrin derivates (6-CD-CTS), which possessed a high cyclodextrin loading capacity (2.12 × 10−4 mol/g), as the carrier. The biosensor was prepared through the inclusion of ferrocene as the electron mediator in a hydrophobic cavity of cyclodextrin and crosslinking catalase (CAT) to 2-NH2 of 6-CD-CTS. The ferrocene-included complex was evaluated by ultraviolet-visible spectrophotometry and thermogravimetric analysis. Its electrochemical behavior was also studied. The impact of the reaction conditions on the CAT immobilization capacity was evaluated. When previous membrane was used to detect the concentration of H2O2 ( CH2O2), we found that the catalysis of CAT and the signal amplification of ferrocene had a major impact on the cyclic voltammograms. The optimal working pH of the modified electrode was 7.0. The peak current ( I) had a linear relationship with the H2O2 concentration (CH2O2) in the range 1.0 × 10−4 to 1.0 × 10−3 mol/L. The linear regression equation was I = 0.00475 CH2O2 − 0.03025. The detection limit was 10−6 mol/L. © 2014 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2015, 132, 41499. [ABSTRACT FROM AUTHOR]