离子色谱法测定乳制品中亚硝酸盐和硝酸盐含量的方法改进

改进GB 5009.33—2016《食品安全国家标准 食品中亚硝酸盐和硝酸盐的测定》中离子色谱法测定乳制品（乳粉、生牛乳）中亚硝酸盐和硝酸盐的方法。乳制品中亚硝酸盐和硝酸盐经超纯水提取后，加入乙酸溶液沉淀蛋白，AS11-HC色谱柱分离，电导检测器检测。结果表明：在本研究条件下，亚硝酸盐和硝酸盐的标准曲线均线性关系良好，相关系数均大于0.99；纯牛乳中亚硝酸盐的定量限为0.25 mg/kg、硝酸盐的定量限为0.8 mg/kg，乳粉中亚硝酸盐的定量限为1 mg/kg、硝酸盐的定量限为5 mg/kg；乳粉和纯牛乳中亚硝酸盐、硝酸盐回收率均能达到80%～110%，方法操作便捷、成本低、回收率理想、精密度较高。该法优化了国标检测方法的条件，解决了其中可能遇到的问题，可以更加快速、准确地检测乳制品中低含量亚硝酸盐和硝酸盐。     

桑黄多糖抗疲劳及耐缺氧实验研究

研究采用水提醇沉法得到桑黄菌丝多糖(大分子量粗多糖),通过小鼠抗疲劳、耐缺氧能力实验,研究桑黄菌丝多糖的生理活性。以小鼠游泳力竭时间、游泳前后血乳酸、肝糖原以及血清尿素氮含量的变化为指标,考察桑黄多糖抗疲劳能力,以小鼠在缺氧和亚硝酸钠中毒环境下的存活时间为指标,考察桑黄多糖耐缺氧能力。结果表明,灌胃桑黄多糖可以显著延长小鼠游泳时间达70.62%,降低游泳后乳酸曲线下面积22.89%,提高肝糖原储备33.36%,减少游泳后血清尿素氮含量23.17%,延长小鼠在缺氧环境下42.08%和亚硝酸钠中毒环境下35.29%的存活时间。因此,桑黄多糖具有提高小鼠抗疲劳和耐缺氧能力的作用,且在一定剂量范围内,实验效果与灌胃剂量呈正效应关系。     

泡菜中亚硝酸盐的研究进展

对泡菜中亚硝酸盐的检测方法、含量变化及影响含量变化的因素、降低亚硝酸盐含量的方法等方面的研究进展进行综述,以期为泡菜的生产提供指导。     

低盐高酸酱腌菜中亚硝酸含量的比较研究

为探讨酱腌菜中亚硝酸盐含量与食盐、酸度等的关系,以丕蓝、白菜、芹菜、甘蓝、豆角等为原料,按不同比例食盐量、醋酸量、腌制温度制成酱腌菜,采用盐酸萘乙二胺分光光度法测定酱腌莱中亚硝酸盐含量。结果显示食盐质量分数为0.51%,酸度为1.18%的新醋腌制的丕篮亚硝酸盐含量最低;食盐质量分数11.61%,酸度为0.03%的酱咸菜亚硝酸盐含量最高。     

食品中亚硝胺类化合物的危害及控制研究进展

亚硝胺是对人类健康危害性极高的化合物之一。本文阐述N-亚硝基化合物的危害及在食品中的分布状况,综述应用辐照和天然植物提取物等阻断剂消除和控制食品中N-亚硝基化合物技术措施的研究进展。     

亚硝酸盐中毒模型小鼠组织器官中VEGF的分布特点

为探讨血管内皮生长因子(VEGF)在小鼠亚硝酸盐中毒组织损伤中的作用,将20只小鼠随机分为对照组和亚硝酸盐中毒组,分别注射0.3mL的生理盐水和50g/L亚硝酸钠。中毒组小鼠死亡后,处死对照组小鼠,采取心、肝、脾、肺、肾、脑等组织,制作石蜡切片,进行HE染色和VEGF免疫组化染色,镜下观察组织病变以及VEGF蛋白的分布特点。结果显示,亚硝酸盐中毒可引起小鼠机体产生明显的缺氧症状,心、肝、脾、肺、肾等组织都有不同程度的病理损伤,主要表现为水肿和出血;各组织均观察到VEGF阳性信号,在出血病变区域阳性信号最为明显。说明亚硝酸盐中毒可造成机体各器官不同程度的病理损伤,并引起小鼠体内VEGF表达量的增加,VEGF对器官的病理变化有明显的促进作用。     

一株产生氨氮和亚硝酸盐氮菌的筛选鉴定及特性研究

从4个草鱼池塘中分离和定性筛选获得29株能够产生氨氮和亚硝酸盐氮的菌株。通过对编号为C95的菌株进行菌落形态学观察和16S rDNA序列分析,表明该菌株为革兰氏阴性杆状菌,与寡养单胞菌属(Stenotrophomonas sp.)的同源性达98%。采用单因素多水平试验对菌株的产氨氮和产亚硝酸盐氮特性进行研究发现:(1)氮源、碳源、温度和摇床转速都能显著影响菌株的生长及产生氨氮和亚硝酸盐氮的含量,但pH(5～9)对其无显著影响(P>0.05);(2)该菌株生长及产生氨氮和亚硝酸盐氮最适宜的培养基以及培养条件为:LB、pH 5～9、25℃、150 r.min-1。由C95作为指示菌株筛选得到SC01、SC07两株(2/33)去除氨氮和亚硝酸盐氮效果较好的菌株。因此,C95可作为筛选具有降氨氮和亚硝酸盐氮功能的有益菌的指示菌株。     

Ability to utilize lactate and related enzymes of a ruminal bacterium, Selenomonas ruminantium

The ability of a nitrate‐reducing and nitrite‐reducing strain of Selenomonas ruminantium ssp. lactilytica (TH1) to utilize lactate was examined at the cell and enzyme levels. The TH1 strain was found to possess NAD‐independent D‐lactate dehydrogenase (iD‐LDH), with little or no lactate racemase or L‐lactate dehydrogenase, implying that TH1 virtually utilizes only the D‐form of lactate. Therefore, the introduction of lactate racemase to TH1 may enhance its ability to utilize lactate in the rumen where both D‐lactate and L‐lactate are produced. Because lactate utilization by Megasphaera elsdenii in the rumen may increase methanogenesis, it is desirable to increase lactate utilization by S. ruminantium, which may decrease methanogenesis. However, the specific activity of iD‐LDH, which represents the amount of enzyme per cell, in TH1 was approximately threefold lower than M. elsdenii. Properties of iD‐LDH, such as optimal pH and temperature, affinity for D‐lactate, and effect of metal ions, did not differ greatly between TH1 and M. elsdenii. The specific activity of iD‐LDH in TH1 increased as the D‐lactate concentration in the medium increased, suggesting that iD‐LDH synthesis is regulated in response to D‐lactate. On the contrary, no iD‐LDH activity was detected when TH1 was grown in the presence of glucose, even when D‐lactate was present. This result suggests that iD‐LDH synthesis is strongly suppressed by glucose. In order to improve the ability of S. ruminantium to utilize lactate and reduce nitrate and nitrite, it is important to enhance iD‐LDH synthesis in addition to the introduction of lactate racemase.     

Nitric Oxide Response in Critically III Dogs

Alterations in nitric oxide (NO)production may play a role in critical illness. Total serum nitrate/nitrite concentrations [SNN (uM/L)], the stable metabolites of NO, have been used as an indirect measure of NO in people, with increased concentrations reported in cases of critical illness. The relationship of nitric oxide (NO) to criticalillness in dgos is unknown. We tested the hypothesis that critically ill intensive care unit (ICU) canine illness in dogs is unknown. We tested the hypothesis that critically ill intesive care unit (ICU) canine patients would have increased SNN as compared to healthy dogs and non-critically ill dogs. An organ failure index score (OFI) was assigned to dogs admitted to the ICU to evaluate trends between disease severtiy and SNN. Critically ill dogs had significantly (p < 0.05) higher SNN (median 10.53) as compared to non-critically ill dogs (median 2.3) and healthy dogs (median 1.92). Critically ill dogs with the most severe disease (as based on OFI) had higher SNN concentrations. Survival of critically ill dogs with SNN of > 15 upon ICU admission (12% survival) was significantly less than survival of critically ill dogs with SNN ≤ 15 (91%) survival).l (Vet. Emerg. & Crit. Care, 9: 195–202, 1999)