壳聚糖包裹CdTe的物理表征及生物毒性研究

选用天然多糖中唯一的碱性多糖-壳聚糖作为稳定剂和包裹剂,成功地在水相中以温和条件合成了粒径小小于10nm的壳聚糖包裹cdTe纳米粒子（CdTe／CS）和壳聚糖微球包裹的CdTe纳米粒子（CdTel／CSMs）,对两种纳米粒子物理表征显示,二者均具有较好的光学性质稳定、发射峰峰位分布范围宽、紫外吸收光谱宽且连续的特点。相比ECdTe的毒性,CdTe／CS和cdTe,CsMs纳米粒子的细胞毒性有明显降低,且生物相容性强,可以应用在生物医学检验、细胞成像,甚至活体研究中。     

食品中氯丙醇污染及其毒性

氯丙醇类化合物,尤其是3-MPCD对酱油污染成为国际上关注食品安全热点问题之一。为了对该类物质有一全面了解,该文对食品中氯丙醇类化合物的种类、特性、来源、毒性、检测方法和预防措施及各国限量标准进行综述。     

纸厂废水中有机化合物分析研究进展

纸厂废水的主要特征有:色度大,悬浮物含量高,臭味大,含高浓营养物(可导致受纳水体富营养化)并且有毒性.本文概述了纸厂废水中的有机化合物,以及其分离提取技术和毒性特征测试方法.     

八角籽仁油GC-MS分析和急性毒性试验

以石油醚为溶剂提取八角籽仁油,通过GC—MS分析了八角籽仁油中脂肪酸的组成及含量,并对八角籽仁油进行了急性毒性试验。结果表明,八角籽仁油中亚油酸含量34．658％,油酸含量34．986％,棕榈酸含量17．838％,山嵛酸含量4．096％,硬脂酸含量4．093％,花生酸含量1．550％,二十四碳酸含量1．336％;不饱和脂肪酸占69．644％,饱和脂肪酸占28．913％。急性毒性试验初步确定八角籽仁油小鼠最小致死量和最大耐受量均大于40mL/kg。     

发光细菌毒性检测机理及应用研究进展

阐述了发光细菌及其检测有毒有害物质的机理,综述了近年来发光细菌在毒性评估及食品安全检测中的应用研究进展,指出了发光细菌应用于食品安全检测过程中的影响因素,并指明了该技术领域应用研究方向。     

唐菖蒲伯克霍尔德菌椰毒致病型菌株Co14毒力相关基因解析

目的了解1株引起致死性食物中毒事件的唐菖蒲伯克霍尔德菌椰毒致病型菌株Co14的全基因组序列特征,对其基因组中米酵菌酸(BA)和毒黄素(TF)的生物合成相关基因进行了预测和分析。方法通过第三代高通量测序技术(PacBio)对Co14进行全基因组测序,使用BLAST软件预测BA和TF的生物合成相关基因。结果 Co14基因组中含有2个闭合的环状染色体,大小分别为4.1和4.0 Mb,鸟嘌呤和胞嘧啶所占比例(GC含量)分别为67.82%和68.32%。Co14基因组中还携带有一个146 kb的闭合环状质粒,GC含量为63.25%,编码149个基因。通过同源序列比对,在Co14染色体1上发现了BA和TF的生物合成相关基因簇bonR1R2LJKFGABDEHIM和toxRABCDE。结论 Co14全基因组数据为研究唐菖蒲伯克霍尔德菌食物中毒菌株的致病性和毒力因子产生机制奠定了遗传学基础。     

龙葵素的生殖毒性研究进展

龙葵素广泛存在于马铃薯、番茄及茄子等茄科植物中。因其具有抗肿瘤和潜在的毒性作用而引起广泛关注。本文主要介绍了龙葵素在生殖毒性方面的研究进展。     

硫丹对鱼类的毒性效应研究进展

总结了硫丹对不同鱼类的急性致死毒性,对鱼类的细胞毒性和组织病理学,对鱼类生理生化指标的影响,以及对鱼类的遗传、繁殖和发育毒性,建议研究硫丹与其他污染物共暴露对鱼类的联合毒性,开展更多的实验来确定硫丹对鱼类的毒性机制,加强鱼类全生命周期暴露、子代传递效应、多代繁殖影响的研究。     

Safety Evaluation and Anti-Inflammatory Efficacy of Lacticaseibacillus paracasei PS23

Lacticaseibacillus paracasei strain PS23 (PS23) exhibits some probiotic properties. In this study, a genomic analysis of PS23 revealed no genes related to virulence or antibiotic resistance. Moreover, ornithine decarboxylase activity was not detected in vitro. In addition, PS23 was sensitive to the tested antibiotics. Genotoxicity tests for PS23 including the Ames test and chromosomal aberrations in vitro using Chinese hamster ovary cells and micronuclei in immature erythrocytes of ICR mice were all negative. Moreover, following a 28-day study involving repeated oral dose toxicity tests (40, 400, and 4000 mg/kg equal 1.28 × 10¹⁰, 1.28 × 10¹¹, and 1.28 × 10¹² CFU/kg body weight, respectively) using an ICR mouse model, no adverse effects were observed from any doses. In addition, supplementation with live or heat-killed PS23 ameliorates DSS-induced colonic inflammation in mice. Our findings suggest that PS23 is safe and has anti-inflammatory effects and may therefore have therapeutic implications.     

Disruption of Membrane Integrity as a Molecular Initiating Event Determines the Toxicity of Polyhexamethylene Guanidine Phosphate Depending on the Routes of Exposure

Polyhexamethylene guanidine phosphate (PHMG-P), a cationic biocide, is widely used in household products due to its strong bactericidal activity and low toxicity. However, it causes fatal lung damage when inhaled. In this study, we investigated why PHMG-P causes fatal lung injury when inhaled, and demonstrated that the disruption of membrane integrity through ionic interaction—a molecular initiating event of PHMG-P—determines toxicity. Mice were injected intravenously with 0.9 or 7.2 mg/kg PHMG-P (IV group), or instilled intratracheally with 0.9 mg/kg PHMG-P (ITI group); they were euthanatized at 4 h and on days 1 and 7 after treatment. Increased total BAL cell count and proinflammatory cytokine production, along with fibrotic changes in the lungs, were detected in the ITI group only. Levels of hepatic enzymes and hepatic serum amyloid A mRNA expression were markedly upregulated in the 7.2 mg/kg IV and ITI groups at 4 h or day 1 after treatment, but returned to baseline. No pathological findings were detected in the heart, liver, or kidneys. To simulate the IV injection, A549, THP-1, and HepG2 cells were treated with PHMG-P in cell culture media supplemented with different serum concentrations. Increased serum concentration was associated with an increase in cell viability. These results support the idea that direct contact between PHMG-P and cell membranes is necessary for PHMG-induced toxicity.