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Peroxidative protection of high lipid : low dextrose parenteral admixture by D ‐α‐tocopherol
Author(s) -
Becvarova I.,
Saker K. E.
Publication year - 2005
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/j.1439-0396.2005.00611_10.x
Subject(s) - lipid peroxidation , chemistry , tocopherol , in vivo , antioxidant , ethanol , food science , chromatography , biochemistry , vitamin e , biology , microbiology and biotechnology
A practical alternative to traditional central line delivery of parenteral admixtures (PA) for small animal patients is utilization of a peripheral route. Admixtures delivered via this route should be a lower osmolarity to prevent complications; to attain this goal a high lipid:low dextrose (HL:LD) is formulated. Lipid peroxidation is a common sequella of PA containing high lipid content. This in vitro peroxidation can lead to oxidative injury of biological membranes in vivo . Despite this concern, peripheral PA have many benefits and continue to be utilized. Therefore, the objectives of this study were to measure lipid hydroperoxides in HL:LD PA; and to determine the optimal dose of d ‐α‐tocopherol to minimize peroxidation in the PA during a 24 h hang time. This in vitro experiment included three identical blocks consisting of 14 bags ( n = 7 control; n = 7 treatment) filled aseptically with 109 ml of HL:LD PA. Total lipid content per bag was 8 g as soybean oil (Intralipid ® ). Natural d ‐α‐tocopherol (Vital E‐300™) was added to the treatment bags as 8, 12, 16, 24, 32, 48, 64 IU/g of lipid. Control bags contained Vital E‐300™ equivalent amounts of ethanol and benzyl alcohol. Bags were hung for 24 h at room temperature under fluorescent light exposure. Hydroperoxides were measured by FOX assay and tocopherols by HPLC at times 0 and 24 h. The level of hydroperoxides was expressed as μM equivalents tert‐butyl hydroperoxide (μM = TBH). A Repeated Measures anova was used for data analysis, with p < 0.05 considered significant. Detectable levels of hydroperoxides were found in all PA at time 0 and 24. Mean TBH concentrations in control bags were 380 and 383 μM at time 0 and 24 respectively. A 3‐way interaction (time x treatment x α‐toc) was observed, p = 0.0018. d ‐α‐tocpherol supplementation at 24–64 IU/g lipid decreased (p < 0.0001) TBH production from controls at time 0. By time 24 h, significant reduction in TBH was observed with Vit E concentrations of 48 and 64 IU/g lipid of d ‐α‐tocopherol. In conclusion: lipid peroxidation of HL:LD PA occurs immediately following lipid administration, and d ‐α‐tocopherol, as Vital E‐300™, appears to significantly minimize this peroxidation process in vitro based on concentration and time of exposure to lipid. This has clinical implications for parenteral feeding in critically ill patients.