从害虫马尾松毛虫中提取甲壳素的初步研究

采用酸碱法对马尾松毛虫蛹中甲壳素的提取方法进行了初步研究。重点分析了N aOH不同处理条件对脱有机物质和甲壳素产率的影响,确定了从马尾松毛虫蛹中提取甲壳素的基本工艺:(1)脱矿物质:盐酸浓度为2.5%,浸泡时间为20 h,浸泡温度为30℃;(2)脱有机物质:N aOH浓度为6%,浸泡温度为75℃,浸泡时间为10 h;(3)脱色:双氧水浓度为9%,浸泡时间为2.5 h,浸泡温度为80℃。在此条件下,获得的甲壳素产品为白色粉状固体,其N含量为6.87%,灰分为1.19%,水分为8.37%。产率为29.97%。产品的N含量达到食品级甲壳素标准,灰分含量达到工业级甲壳素标准。实验有助于后续深入研究马尾松毛虫蛹中甲壳素的提取,也为今后进一步制备虫蛹壳聚糖打下了基础。     

Effect of a Single Dose of Cadmium on Pregnant Wistar Rats and their Offspring

Cadmium (Cd) is a well‐known toxicant targeting many organs, among them placenta. This heavy metal also has embryonary and foetal toxicity. This study was undertaken to analyse the effect of a single Cd dose administered at 4, 7, 10 or 15 days of gestation on the offspring of pregnant rats sacrificed at 20 days of gestation. Cadmium chloride was administered subcutaneously at 10 mg/kg body weight to Wistar pregnant dams; control animals received a proportionate volume of sterile normal saline by the same route. Maternal uteri, livers, kidneys and lungs, and foetuses were examined at necropsy. Samples of maternal organs and whole foetuses were collected for histopathologic examination, determination of Cd levels and staining by the Alizarin red S technique. Results revealed a clear embryotoxic and a teratogenic effect of this heavy metal, the former as a significant increase in the number of resorptions, and the latter as significant decrease of the gestational sac weight, and the size and weight of foetuses of Cd‐treated dams as well as induced malformations in skull bones, vertebrae and thoracic, and pelvian limbs. The deleterious effects found were similar to those previously reported for other animal models suggesting a high conservation of the pathogenic mechanisms of Cd. Additionally, many of the addressed aspects showed a slight dependence on the time of administration of the toxic that might be due to the accumulation of the metal in different organs, as we were able to demonstrate by the analysis of its concentration.     

Serum markers of lipid peroxidation, antioxidant enzymatic defense, and collagen degradation in an experimental (Pond-Nuki) canine model of osteoarthritis

BACKGROUND:Chondrocyte lipid peroxidation is strongly suggested to mediate collagen degradation and thus, to be involved in the pathogenesis of cartilage degradation and osteoarthritis (OA). OBJECTIVES: The objective of this study was to evaluate early changes in serum biochemical indicators of oxidative stress during the development of OA in a canine model. METHODS: Experimental OA was induced in 7 dogs by transection of the anterior cruciate ligament (Pond-Nuki model). Venous blood samples were obtained prior to the operation and on postoperative days 30, 60, and 105. The activity of serum catalase (an antioxidant enzyme), malondialdehyde (MDA) concentration (a marker of lipid peroxidation), and serum C2C neoepitope concentration (a marker of collagen type II degradation) were measured. RESULTS: A statistically significant increase in all parameters as early as the 30th postoperative day was observed, compared with preoperative values. Serum catalase activity peaked on day 60, whereas MDA and C2C concentrations increased continuously until the end of the experimental period. A significant positive correlation was found between MDA and C2C concentrations, but not between catalase activity and MDA or C2C concentrations. CONCLUSIONS: The results support the hypothesis that oxidative stress is involved in the pathogenesis of OA in the dog based on the Pond-Nuki model. The correlation between MDA and C2C concentrations suggests a possible association between oxidative stress and cartilage degeneration.