Vitamin C (ascorbic acid) is a non-enzymatic antioxidant important in protecting the lung against oxidative damage and is decreased in lung lining fluid of horses with airway inflammation. To examine possible therapeutic regimens in a species with ascorbate-synthesising capacity, ... Te effects of oral supplementation of two forms of ascorbic acid, (each equivalent to 20 mg ascorbic acid per kg body weight) on the pulmonary and systemic antioxidant status of six healthy ponies in a 3 x 3 Latin square design. Two weeks supplementation with ascorbyl palmitate significantly increased mean plasma ascorbic acid concentrations compared to control (29 +/-- 5 and 18 +/- 7 umol/L, respectively; p < 0.05). Calcium ascorbyl-2-monophosphate, a more stable form of ascorbic acid, also increased mean plasma ascorbic acid concentrations, but not significantly (23 +/- 1 umol/L; p = 0.07). The concentration of ascorbic acid in bronchoalveolar lavage fluid increased in five out of six ponies following supplementation with either ascorbyl palmitate or calcium ascorbyl-2-monophosphate compared with control (30 +/- 10, 25 +/- 4 and 18 +/- 8 umol/L, respectively; p < 0.01). Neither supplement altered the concentration of glutathione, uric acid or alpha-tocopherol in plasma or bronchoalveolar lavage fluid. In conclusion, the concentration of lung lining fluid ascorbic acid is increased following ascorbic acid supplementation (20 mg/kg body weight) in an ascorbate-synthesising species.
It has been known that solid lipid nanoparticles (SLN) and nanostructured lipid carriers (NLC) have occlusive effects, but ascorbyl palmitate (AP) incorporation moisturized skin significantly better than placebo in short-term (p < 0.001) and long-term trials (p < 0.01) for both SLN and NLC. In the second part of the study, SLN and NLC were found to sustain the penetration of AP through excised human skin about 1/2 and 2/3 times compared to NE (p < 0.001 and p < 0.01), respectively...
6-O-Palmitoyl-L-ascorbic acid dissolved in a sodium taurocholate solution was hydrolyzed by homogenates of the pancreas, liver, and intestines of guinea pigs.
Male MEl mice in which hepatotoxicity had been induced by the feeding of 600 mg/kg acetaminophen had covalent binding of acetaminophen metabolites to hepatic proteins, a depletion of hepatic nonprotein sulphydryl groups after 2 hours, and a dramatic increase in plasma alanine aminotransferase activity after 24 hours. The coadministration of acetaminophen and ascorbyl palmitate reduced this binding within 2 and 4 hours (to 31% and 22%, respectively), reduced the depletion in nonprotein sulfhdryl groups and aminotransferase activity, and completely prevented the 35% mortality observed at 24 hours after acetaminophen treatment alone. Ascorbyl palmitate appeared to prevent hepatic damage by removing the reactive acetaminophen metabolites and by having a sparing action on reduced hepatic glutathione.
Ascorbyl palmitate when topically applied at small doses inhibited 12-O-tetradecanoylphorbol-13-acetate-induced (TPA-induced) ornithine decarboxylase activity, tumor production, and DNA synthesis in mouse epithelial cell. A dose of 4 umol of ascorbyl palmitate inhibited by 60-70% after one topical application of 2 nmol TPA. When 5 nmol TPA was administered with 5 pmol ascorbyl palmitate twice weekly to previously initiated mice, 91% of tumors were inhibited per mouse.
... This work ... sought to determine the antioxidative properties of a lipid-soluble derivative of ascorbic acid, ascorbic acid-6-palmitate. ... Ascorbic acid-6-palmitate reduced cellular levels of reactive oxygen species following ultraviolet B irradiation. Treatment of keratinocytes with ascorbic acid-6-palmitate inhibited ultraviolet-B-mediated activation of epidermal growth factor receptor, extracellular regulated kinases 1 and 2, and p38 kinase because of its ability to prevent reduced glutathione depletion and scavenge hydrogen peroxide. Ascorbic acid-6-palmitate strongly promoted ultraviolet-B-induced lipid peroxidation, c-Jun N-terminal kinase activation, and cytotoxicity, however. End products of lipid peroxidation, such as 4-hydroxy-2-nonenal, have been reported to mediate stress-activated protein kinase activation and cell toxicity in epithelial cells. The lipid component of ascorbic acid-6-palmitate probably contributes to the generation of oxidized lipid metabolites that are toxic to epidermal cells. /The/ data suggest that, despite its antioxidant properties, ascorbic acid-6-palmitate may intensify skin damage following physiologic doses of ultraviolet radiation.
来源:Hazardous Substances Data Bank (HSDB)
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研究了包括抗坏血酸棕榈酸酯在内的各种抗氧化剂对兔血小板功能的影响，通过血栓素B2合成和酶免疫分析法进行。抗坏血酸棕榈酸酯在1.0 X 10-5 M及以上浓度时抑制了A-23187诱导的血栓素B2合成，并在同时添加时在1. X 10-7 M浓度下抑制了凝血酶诱导的合成。当血小板预先用抗坏血酸棕榈酸酯处理后，也抑制了两种激动剂诱导的合成，除非血小板已被凝血酶刺激。当兔子连续5天摄入抗坏血酸棕榈酸酯的ADI（人体可接受日摄入量）浓度时，激动剂诱导的血小板活化也显著减少。
... The effects of various antioxidants, including ascorbyl palmitate, on rabbit platelet functions /were studied/ by means of thromboxane B2 synthesis and enzyme immunoassay. Ascorbyl palmitate inhibited A-23187-induced thromboxane B2 synthesis at 1.0 X 10-5 M and above, and thrombin-induced synthesis at 1. X 10-7 M when added simultaneously. The pretreatment of platelets with ascorbyl palmitate also inhibited both agonist-induced syntheses unless the platelets had been stimulated with thrombin. When the rabbits were fed ADI concentrations of ascorbyl palmitate for 5 days, agonist-induced activation of platelets also was reduced considerably.
/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/
When incorporated into the cell membranes of human red blood cells, ascorbyl palmitate has been found to protect them from oxidative damage and to protect alpha-tocopherol (a fat-soluble antioxidant) from oxidation by free radicals. However, the protective effects of ascorbyl palmitate on cell membranes have only been demonstrated in the test tube. Taking ascorbyl palmitate orally probably doesn't result in any significant incorporation into cell membranes because most of it appears to be hydrolyzed (broken apart into palmitate and ascorbic acid) in the human digestive tract before it is absorbed. The ascorbic acid released by the hydrolysis of ascorbyl palmitate appears to be as bioavailable as ascorbic acid alone.
When applied topically to guinea pigs, ascorbyl palmitate penetrated the skin barrier so that ascorbic acid content in the skin, liver, and blood increased eight-, seven-, and four-fold, respectively, when compared to control animals that did not receive ascorbyl palmitate.
(14)C-Ascorbyl palmitate was applied to the skin of scorbutic (affected by scurvy) guinea pigs. Following the topical application, ascorbic acid concentrations in the skin, liver, kidneys, and blood were four to eight times greater than in the control.
Ascorbyl palmitate dissolved in a sodium taurocholate solution was hydrolyzed by homogenates of the liver, pancreas, and intestines of guinea pigs. Approximately 80% of ascorbyl palmitate was hydrolyzed to free ascorbic acid by homogenates of the small intestine and pancreas. ... Ascorbyl palmitate (the equivalent of 20 mg of ascorbic acid) was orally administered to guinea pigs, and the amount of free ascorbic acid excreted in the urine was measured. Greater amounts of acid were excreted at 0-24 hours than at 24-48 hours. A similar trend was found in these organs of free ascorbic acid content when L-ascorbic acid was administered instead, but a reverse tendency was observed with ascorbyl palmitate.
