In most clinical laboratories, low density lipoprotein (LDL) cholesterol is usually estimated indirectly with the Friedewald equation or directly with the N-geneous assay. We assessed LDL-cholesterol values obtained by both methods to find an appropriate fasting period and to assess the influence of the energy content of the last meal. Blood samples were taken from 28 healthy volunteers who had consumed a standard meal (107 g of carbohydrate, 658 kcal) followed by a fasting period of 12 and 18 h, or a high-energy meal (190 g of carbohydrate, 1011 kcal) with a fasting period of 12 h. Prolongation of the fasting period from 12 h to 18 h decreased glucose level, but did not decrease triacylglycerol, total cholesterol, or high density lipoprotein (HDL) cholesterol. LDL-cholesterol levels measured with the N-geneous assay did not change (94.0 ± 21.5 to 96.3 ± 19.1 mg/dl). LDL-cholesterol levels calculated with the Friedewald equation were also similar after fasting periods of 12 h (98.5 ± 21.4 mg/dl) and 18 h (99.7 ± 20.2 mg/dl). The high-energy meal did not change the level of LDL-cholesterol measured with the N-geneous assay (96.1 ± 21.2 mg/dl), or the glucose, triacylglycerol, total cholesterol, or HDL-cholesterol level, but LDL-cholesterol levels evaluated from the Friedewald equation (92.6 ± 20.3 mg/dl) became significantly lower. A fasting time longer than 12 h is not necessary to obtain reasonable blood lipid levels. The Friedewald equation gave higher LDL-cholesterol levels than N-geneous assay in young Japanese females who had eaten a low-energy meal, and lower values when they had eaten a high-energy meal. Thus, it may be necessary to pay attention to energy of nigh meal prior to blood withdrawal.
Since we have been exposed to excessive amounts of stressors, aromatherapy for the relaxation has recently become very popular recently. However, there is a problem which responds to light with the essential oil used by aromatherapy. It is generally believed that singlet oxygen is implicated in the pathogenesis of various diseases such as light-induced skin disorders and inflammatory responses. Here we studied whether essential oils can effectively scavenge singlet oxygen upon irradiation, using the electron spin resonance (ESR) method. Green light was used to irradiate twelve essential oils from rutaceae. Among these twelve essential oils, eight were prepared by the expression (or the compression) method (referred to as E oil), and four samples were prepared by the steam distillation method (referred to as SD oil). Five E oils enhanced singlet oxygen production. As these essential oils may be phototoxic, it should be used for their use whit light. Two E oils and three SD oils showed singlet oxygen scavenging activity. These results may suggest that the antioxidant activity of essential oils are judged from their radical scavenging activity. Essential oils, which enhance the singlet oxygen production and show higher cytotoxicity, may contain much of limonene. These results suggest that limonene is involved not only in the enhancement of singlet oxygen production but also in the expression of cytotoxic activity, and that attention has to be necessary for use of blended essential oils.
Ischemia-reperfusion injury associated with liver transplantation remains a serious complication in clinical practice. In the present study the effect of intake of α-tocopherol or β-carotene to limit liver injury by oxidative stress in ischemia and reperfusion was explored. Wistar rats were fed with diets enriched with α-tocopherol (20 mg/day) or β-carotene (3 mg/day) for 21 days. After 21 days, their livers were subjected to 15 and 30 min of ischemia and afterwards were reperfused for 60 min. The recovery of levels of ATP during reperfusion was better in the group of rats whose diets were supplemented with α-tocopherol or β-carotene than in the group control. The supplementation of the diet induced changes in the profile of enzymatic antioxidants. The supplementation with α-tocopherol and β-carotene resulted in a decreased of superoxide dismutase during the ischemia and a recovery was observed after reperfusion. Not changes were observed for the enzymes catalase and glutathione peroxidase and glutathione but their values were higher to those of the group control. In conclusion, the supplementation with α-tocopherol and β-carotene improve the antioxidant and energetic state of liver after ischemia and reperfusion injury.
Effects of azuki bean juice supplementation, prescribed according to a Kanpo medicine regimen, on serum lipid concentrations were studied. Healthy young Japanese women were recruited and were randomly assigned to one of the three groups using a parallel-group design. Control (n = 10), azuki (n = 11) and Concentrated azuki (CA) (n = 12) juice groups consumed 150 g daily of the isocaloric assigned juice for one menstrual cycle with their usual diet. Triglyceride concentrations were decreased in the azuki juice group (p<0.05) and tended to be decreased in the CA juice group (p = 0.055). Triglyceride concentrations in the azuki and CA juice groups decreased by 0.170 mmol/liter (15.4%) and 0.159 mmol/liter (17.9%), respectively (p<0.05). The azuki and CA juice used in this study inhibited pancreatic lipase activity 29.2% and 56.9%, respectively, in vitro. Lipid peroxide changes, based on ANCOVA with the initial level and α-tocopherol changes as covariates, did not differ among the three groups. Serum low density lipoprotein-cholesterol and high density lipoprotein-cholesterol (HDL) cholesterol concentrations did not change. Thus, azuki bean juice intake, as a traditional Kampo prescription, might be beneficial for preventing hypertriglyceridemia.
During the lipid peroxidation reaction, lipid hydroperoxides are formed as primary products. Several lines of evidence suggest that lipid hydroperoxides can trigger cell death in many cell types, including neurons. In a screening of lipid hydroperoxides which can induce toxicity in neuronal cells, we found docosahexaenoic acid hydroperoxides (DHA-OOH) induced much severe levels of reactive oxygen species generation and cell death in human neuroblastoma SH-SY5Y cells compared to the hydroperoxides of linoleic acid and arachidonic acid. Therefore, we focused on DHA-OOH, and demonstrated that DHA-OOH apparently induced an apoptosis in the neuronal cells through several apoptotic hallmarks including nuclei condensation, DNA fragmentation, poly (ADP-ribose) polymerase cleavage and increased activity of caspase-3. We also found the signaling changes in mitochondria-mediated apoptosis, such as cytochrome c release and increased expression of Bcl-2, as well as a dose-dependent attenuation of mitochondrial membrane potential in the DHA-OOH treated cells. These data indicated DHA hydroperoxide as a potential inducer of apoptosis in human neuroblastoma SH-SY5Y cells, which may be mediated by mitochondria dysfunction pathway.
The clinical efficacy of gastroprotective drugs or low-dose H2 receptor antagonists in the prevention of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy is limited. The aim of the present study was to investigate efficacy of rebamipide and famotidine in Helicobacter pylori (H. pylori)-negative healthy volunteers taking NSAID. This study was a randomized, two way crossover study comparing the preventive effect rebamipide 100 mg, t.i.d. and famotidine 10 mg, b.i.d against indomethacin (25 mg, t.i.d.)-induced gastric mucosal injury in H. pylori-negative healthy volunteers. 12 subjects satisfied criteria and were randomized. Endoscopy was performed at baseline and again after the treatment for 7 days, and symptoms were recorded during the treatment. Tissue levels of lipid peroxides and myeloperoxidase and serum indomethacin concentrations were also measured. Subjective symptoms were developed in 58% (7/12) of the rebamipide group, and in 75% (9/12) of the famotidine group (no significant differences). The incidence of gastric lesions (modified Lanza score 2 or higher) was 17% (2/12) in the rebamipide group and 25% (3/12) in the famotidine group. Peptic ulcers did not occur in both groups. There were no significant differences in tissue levels of lipid peroxide and myeloperoxidase and serum level of indomethacin between two groups after the treatment. In conclusion, these data recommend rebamipide (100 mg, t.i.d.) or famotidine (10 mg, b.i.d.) for the prevention of acute gastric injury induced by NSAID in patients without a particular risk factor.
To elucidate the radiosensitivity of an acatalasemic mouse, we examined the time and dose-dependency in the survival rates, the lymphocytes and the intestinal epithelial cells, and the antioxidant function after 3.0 to 12.0 Gy whole body irradiation. Results showed that no significant differences between acatalasemic mice and normal mice were observed in the survival rates and the histological changes in spleens and small intestine after each irradiation. The catalase activities in livers and spleens of acatalasemic mice were significantly lower than those of normal mice and the glutathione peroxidase activity in livers of acatalasemic mice was significantly higher than that of normal mice. At 10 days after 6.0 Gy irradiation, the catalase activities in livers of acatalasemic and normal mice and that in spleens of normal mice significantly decreased compared with no-irradiation control, and there were no differences between those catalase activities. The total glutathione content in acatalasemic mice was significantly higher than that in normal mice at 10 days after 6.0 Gy irradiation. These findings suggested that the radiosensitivity of acatalasemic mice in terms of whole body irradiation doesn’t significantly differ from that of normal mice, probably due to compensated sufficient contents of glutathione peroxidase and total glutathione in acatalasemic mice.