Limiting light-induced lipid peroxidation and vitamin loss in infant parenteral nutrition by adding multivitamin preparations to Intralipid

Parenteral lipids are susceptible to light-induced peroxidation, particularly under phototherapy. Ascorbic acid is protective. The aim of this study was to investigate whether dark delivery tubing and/or coadministration of multivitamin preparations could prevent peroxidation of Intralipid without undue vitamin loss. In experiments carried out on the benchtop, lipid peroxidation occurred in ambient light and was more extensive under phototherapy. Dark tubing decreased peroxide formation, but only by about 65%. In simulated clinical conditions in which solutions were pumped through standard clear or dark minibore plastic tubing, Intralipid accumulated lipid peroxides as measured by the FOX assay (280 µM) or as triglyceride hydroperoxides (52 µM). Multivitamin preparations (MVIP or completely, and were fully protective when used with dark tubing. There was loss of riboflavin (65% from Soluvit and 35% from MVIP) in clear tubing but this was decreased to 18% and 11%, respectively, in dark tubing. Ascorbate loss was 20% (MVIP) and 50% (Soluvit) and only slightly less in dark tubing. Ascorbate loss was also seen in the absence of Intralipid and is due to riboflavin-induced photo-oxidation.Conclusion: Multivitamin preparations protect Intralipid against light-induced formation of lipid hydroperoxides, and administering multivitamins with Intralipid via dark delivery tubing provides a practical way of preventing peroxidation of the lipid while limiting vitamin loss. This procedure should be considered for routine use as well as with phototherapy. Soluvit/Vitlipid) inhibited peroxide formation almost     

营养干预对微波致大鼠海马过氧化损伤的保护效应研究

目的 观察微波急慢性辐照对大鼠海马的过氧化损伤效应,探讨微量营养素干预对微波致海马过氧化损伤的保护作用。方法 急性辐照组采用65W/cm²微波辐照20min后用营养饲料喂养八周,慢性辐照组采用15W/cm²微波辐照每天20min,连续8周,通过生化检测SOD、MDA、GSH-PX和ROS评价海马过氧化损伤。结果 微波急慢性辐照均能引起各组别大鼠海马SOD活性、GSH-PX活性、抑制ROS能力下降(P<0.05),MDA含量增加(P<0.05);而营养干预在微波急慢性辐照时能够显著保护SOD、GSH-PX活性(P<0.05),减少MDA含量(P<0.05),有效地促进抑制ROS能力的恢复(P<0.05)。结论 微波急慢性辐照均导致大鼠海马脑组织过氧化损伤,微量营养素干预能通过抗氧化对微波导致的海马组织损伤发挥保护作用。     

Evidence of oxidative stress in the renal cortex of diabetic rats: favourable effect of vitamin E

The aim of this study was to determine whether there are any disturbances of red/ox balance in the renal cortex of rats during the course of experimental diabetes. In the renal cortex of rats with streptozotocin-induced diabetes, the activity of superoxide dismutase (SOD) isoenzymes, glutathione peroxidase (GSH-Pox), glutathione S-transferase (GST) and glutathione reductase (GSH-RED) was measured in the 5th, 10th and 15th weeks of diabetes. Free radical cell damage was assessed on the basis of malonyldialdehyde (MDA) concentration. The influence of lipophilic antioxidant vitamin E on these analytes was also studied. An increase in MDA concentration in the 10th and 15th weeks of diabetes correlated significantly with plasma glucose concentration (r = 0.47; p < 0.001). Moreover, MDA concentration was influenced by time (+); p < 0.001, diabetes (+); p < 0.001, vitamin E (-) p < 0.001 (ANOVA). Plasma creatinine concentration in rats was elevated by diabetes (p < 0.001), whereas vitamin E decreased the concentration (p < 0.05). Vitamin E lowered the activity of GSHPox (p < 0.001) and GST (p < 0.01) (ANOVA). Our results indicate that during experimental diabetes, disturbances of red/ox balance lead to disturbance in renal function manifested as increased creatinine blood concentration. We suggest that oral supplementation of vitamin E protects the renal cortex of rats during experimental diabetes.     

维生素E对乙醇性肝损伤大鼠肝线粒体SOD和MDA的影响

目的:研究维生素E在乙醇性肝损伤肝组织亚细胞水平上的作用。方法:采用乙醇性肝损伤大鼠模型,测定乙醇灌胃及其VitE处理后肝线粒体SOD、MDA。结果:乙醇灌胃后肝线粒体SOD下降,而MDA上升;维生素E处理后SOD明显上升,MDA下降。结论:VitE可使乙醇性肝损伤大鼠肝线粒体SOD、MDA趋向正常,有抗氧化作用。     

抑肽酶对四氯化碳所致急性肝损伤小鼠体内脂质过氧化的影响

目的研究抑肽酶对四氯化碳所致急性肝损伤小鼠体内脂质过氧化的影响。方法以四氯化碳诱导小鼠急性肝损伤模型，测定各组肝损伤小鼠血清超氧化物岐化酶（SOD）、丙二醛（MDA）、还原型谷胱甘肽（GSH）水平，同步观察抑肽酶对急性肝损伤小鼠体内脂质过氧化反应及肝脏病理改变的影响。结果抑肽酶可明显升高小鼠血清SOD、GSH水平，降低MDA水平，肝脏病理学检查亦表明抑肽酶使肝细胞变性坏死程度减轻。结论提示抑肽酶通过抗脂质过氧化的作用发挥对急性肝损伤的保护作用。     

不同补铁方法对维持性血液透析患者贫血、炎症及氧化应激的影响

目的探讨维持性血液透析患者由口服铁剂改为静脉铁剂前后贫血、炎症及氧化应激反应的变化。方法选择北京大学第三医院肾内科72名维持性血液透析患者，服速立菲0．6g／d、注射重组人促红细胞生成素（rHuEP0）（9000-12000）IU／w2年半以上，血红蛋白（Hb）仍低于100g／L，改为静脉点滴科莫非或森铁能100mg（每次透析时）至预计总缺铁量，然后每2～3周静脉点滴100mg维持24个月以上，如果Hb大于130g／L减1／4 rHuEP0用量，回顾分析口服治疗和静脉治疗初、12个月和24个月连续3个月患者Hb、血清转铁蛋白饱和度（TSAT）、铁蛋白（SF）、rHuEP0用量，以及血清白介素6（IL-6）、肿瘤坏死因子α（TNFα）、C反应蛋白（CRP）、丙二醛（MDA）的变化。结果口服治疗2年中，患者平均rHuEP0用量（9863±655）IU／w，Hb（95．60±9．74）g／L，TSAT（15．30±2．45）％，治疗初、12个月、24个月比较差异均无显著性（P〈0．05）。改用静脉铁剂后2年中，患者平均rHuEP0用量减少至（7416±437）IU／w，Hb上升至（122．60±11．60）g／L，TSAT上升至（31．30±3．35）％，与口服铁剂相比差异均有显著性（P〈0．05），其中治疗12个月和24个月较治疗初差异均有显著性（P〈0．05），但治疗24个月较12个月差异无显著性（P〉0．05）。IL-6、TNFα在口服或静脉补铁期间、改用静脉铁剂前后变化均无显著性（P〉0．05），MDA在口服铁剂期间变化无显著性，平均值（7．83±4．85）ng／ml，改为静脉铁剂后上升至（13．42±7．15）ng／ml（P〈0．05），其中治疗12个月较治疗初显著升高（P〈0．05），24个月较12个月差异无显著性（P〉0．05）。SF在改用静脉铁剂前后变化无显著性（P〉0．05）。结论维持性血液透析患者由口服铁改为静脉铁2年后贫血纠正，铁缺乏改善，炎症反应无明显变化，氧化应激反应加重。     

Long-term exogenous melatonin treatment modulates overall feed efficiency and protects ovarian tissue against injuries caused by ethanol-induced oxidative stress in adult UChB rats

Background: Chronic ethanol intake leads to reproductive damage including reactive oxygen species formation, which accelerates the oxidative process. Melatonin is known to regulate the reproductive cycle, food/liquid intake, and it may also act as a potent antioxidant indoleamine. The aim of this study was to verify the effects of alcoholism and melatonin treatment on overall feed efficiency and to analyze its protective role against the oxidative stress in the ovarian tissue of UChB rats (submitted to 10% [v/v] voluntary ethanol consumption). Methods: Forty adult female rats (n = 10/group) were finally selected for this study: UChB Co: drinking water only; and UChB EtOH: drinking ethanol at 2 to 6 ml/100 g/d + water, both receiving 0.9% NaCl + 95% ethanol 0.04 ml as vehicle. Concomitantly, UChB Co + M and UChB EtOH + M groups were infused with vehicle + melatonin (100 μg/100 g body weight/d) intraperitoneally over 60 days. All animals were euthanized by decapitation during the morning estrus (4 am ). Results: Body weight gain was reduced with ethanol plus melatonin after 40 days of treatment. In both melatonin‐treated groups, it was observed a reduction in food‐derived calories and liquid intake toward the end of treatment. The amount of consumed ethanol dropped during the treatment. Estrous cycle was longer in rats that received both ethanol and melatonin, with prolonged diestrus. Following to oxidative status, lipid hydroperoxide levels were higher in the ovaries of ethanol‐preferring rats and decreased after melatonin treatment. Additionally, antioxidant activities of superoxide dismutase, glutathione peroxidase activity, and glutathione reductase activity were increased in melatonin‐treated groups. Conclusions: We suggest that melatonin is able to affect feed efficiency and, conversely, it protects the ovaries against the oxidative stress arising from ethanol consumption.     

介入治疗中X线对先天性心脏病患儿过氧化损伤的影响

目的探讨介入治疗中X线电离辐射对先天性心脏病患儿的脂质过氧化损伤及抗氧化功能的影响。方法抽取2010年6月至2011年8月接受先天性心脏病介入诊疗的患儿67例,分别测定先天性心脏病患儿术前、术后2 h血清中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量。结果先天性心脏病患儿术后2 h SOD活力(114.3±14.7)U/mL低于术前(133.6±18.6)U/mL;MAD含量(3.5±1.0)μmol/ml显著高于术前(3.1±1.0)μmol/mL,差异均有统计学意义(P<0.01)。随着照射剂量的增加,SOD活力有逐渐下降的趋势,呈显著负相关(r=-0.68,P<0.05),同时MDA含量有逐渐上升的趋势,呈显著正相关(r=0.75,P<0.05)。结论介入治疗中X线可能使先天性心脏病患儿体内产生过多的自由基,造成机体的过氧化损伤。因此,临床应用中应加强对患儿介入治疗的保护。