She-Ching Wu

Mutagenicity and identification of mutagenic compounds of fumes obtained from heating peanut oil

Since the fume of cooking oil has been reported to increase the risk of lung cancer, the objectives of this study were to evaluate the mutagenicity and to find the mutagens in the fumes of peanut oil heated to the smoke point. Peanut oil prepared from roasted peanut kernel showed a lower smoke point, less unsaturated fatty acids, more fume formation, and stronger mutagenicity than that from unroasted kernel. Further investigation of mutagenic compounds was performed by the Ames test and gas chromatography/mass spectrometry analysis. Among the 12 compounds identified from the neutral fraction of methanol extract, four compounds at a dose of 10 microg per plate were mutagenic to Salmonella Typhimurium TA98 and TA100 in the order of trans-trans-2,4-decadienal > trans-trans-2,4-nonadienal > trans-2-decenal > trans-2-undecenal. Results report the enal compounds formed as the mutagens in the fumes of peanut oil and indicate that inhaling cooking fumes might cause carcinogenic risk.

Fagopyrum tataricum (buckwheat) improved high-glucose-induced insulin resistance in mouse hepatocytes and diabetes in fructose-rich diet-induced mice.

Fagopyrum tataricum (buckwheat) is used for the treatment of type 2 diabetes mellitus in Taiwan. This study was to evaluate the antihyperglycemic and anti-insulin resistance effects of 75% ethanol extracts of buckwheat (EEB) in FL83B hepatocytes by high-glucose (33 mM) induction and in C57BL/6 mice by fructose-rich diet (FRD; 60%) induction. The active compounds of EEB (100 μg/mL; 50 mg/kg bw), quercetin (6 μg/mL; 3 mg/kg bw), and rutin (23 μg/mL; 11.5 mg/kg bw) were also employed to treat FL83B hepatocytes and animal. Results indicated that EEB, rutin, and quercetin + rutin significantly improved 2-NBDG uptake via promoting Akt phosphorylation and preventing PPARγ degradation caused by high-glucose induction for 48 h in FL83B hepatocytes. We also found that EEB could elevate hepatic antioxidant enzymes activities to attenuate insulin resistance as well as its antioxidation caused by rutin and quercetin. Finally, EEB also inhibited increases in blood glucose and insulin levels of C57BL/6 mice induced by FRD.

Hepatoprotection of emodin and Polygonum multiflorum against CCl4-induced liver injury

Context: Polygonum multiflorum is known as a medicinal plant. It has been used as a folk medicine which showed antioxidative property. Objective: Protective effects of the water extracts (w/v:1/10) from fresh P. multiflorum (WEP) on carbon tetrachloride (CCl4)-induced liver damage in rats were investigated. Materials and methods: CCl4 was used for inducing liver damage of SD rats, and WEP and emodin were fed for eight consecutive weeks. Results: We found that emodin levels in fresh WEP was higher than that in ripening WEP. Rats were administered WEP and emodin, the main active compound, for 56 consecutive days. WEP significantly lowered the serum levels of hepatic enzyme markers, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and reduced the generation of malonaldehyde. Treatment with WEP recovered glutathione S-transferase and catalase activity in rats as compared to treatment with CCl4 alone. In addition, serum tumor necrosis factor-α, an inflammatory marker, was found to decrease in rats treated with WEP. In histopathological evaluation, fatty degeneration and necrosis were found to be significantly decreased in the CCl4 plus WEP treatment group. Discussion and conclusion: WEP may be effective in attenuating liver damage by reducing lipid peroxidation as well as by positively modulating inflammation.

Effect of pigeon pea (Cajanus cajan L.) on high-fat diet-induced hypercholesterolemia in hamsters.

Obesity is associated with increased systemic and airway oxidative stress, which may result from a combination of adipokine imbalance and antioxidant defenses reduction. Obesity-mediated oxidative stress plays an important role in the pathogenesis of dyslipidemia, vascular disease, and nonalcoholic hepatic steatosis. The antidyslipidemic activity of pigeon pea were evaluated by high-fat diet (HFD) hamsters model, in which the level of high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), total cholesterol (TC), and total triglyceride (TG) were examined. We found that pigeon pea administration promoted cholesterol converting to bile acid in HFD-induced hamsters, thereby exerting hypolipidemic activity. In the statistical results, pigeon pea significantly increased hepatic carnitine palmitoyltransferase-1 (CPT-1), LDL receptor, and cholesterol 7α-hydroxylase (also known as cytochrome P450 7A1, CYP7A1) expression to attenuate dyslipidemia in HFD-fed hamsters; and markedly elevated antioxidant enzymes in the liver of HFD-induced hamsters, further alleviating lipid peroxidation. These effects may attribute to pigeon pea contained large of unsaturated fatty acids (UFA; C18:2) and phytosterol (β-sitosterol, campesterol, and stigmasterol). Moreover, the effects of pigeon pea on dyslipidemia were greater than β-sitosterol administration (4%), suggesting that phytosterone in pigeon pea could prevent metabolic syndrome.

Improvement of the hypocholesterolemic activities of two common fruit fibers by micronization processing.

This study investigated and compared the potential hypocholesterolemic activities of different insoluble fibers (IFs) prepared from carambola and orange pomace with or without micronization processing. After micronization, the cation-exchange and water-holding capacities of these pectic polysaccharide-rich IFs were effectively increased (from 140 to 180% and from 260 to 290%, respectively). The abilities of these microsized fruit IFs to lower the concentrations of serum triglyceride (by 15.6-17.8%) and serum total cholesterol (by 15.7-17.0%) were significantly (p < 0.05) improved, possibly by means of enhancing the excretion of cholesterol (123-126%) and bile acids (129-133%) in feces. Fecal moisture content was also increased (127-131%) by the consumption of microsized IFs. These results demonstrated that particle size is an important factor in affecting the characteristics and physiological functions of insoluble fibers. The approach of micronization processing might offer the industry an opportunity to improve the physiological functions of food fibers in fiber-rich functional food applications.

Hepatoprotection of Graptopetalum paraguayense E. Walther on CCl4-induced liver damage and inflammation

AIM OF THIS STUDY Graptopetalum paraguayense E. Walther, a vegetable consumed in Taiwan, has been used in folk medicine for protection against liver injury, although its actual efficacy remains uncertain. Therefore, we investigated the protective effects of Graptopetalum paraguayense E. Walther against carbon tetrachloride (CCl(4))-induced liver damage in rats. MATERIALS AND METHODS Water extracts of Graptopetalum paraguayense E. Walther (WGP) were administered for 8 consecutive weeks to male Sprague-Dawley rats. And a dose-dependent manner in preventing liver damage was confirmed. Moreover, the major ingredient of WGP, gallic acid, was also orally administrated in the CCl(4)-induced rats. The hepatoprotective activity was assessed using various biochemical parameters such as antioxidant enzymes and histopathological studies. RESULTS WGP ranging from 50 to 300 mg/kg bw administrations significantly lowered serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, and inhibited malondialdehyde (MDA) generation in CCl(4)-treated rats. WGP increased cellular GSH level and antioxidant enzymes, including superoxide dismutase, glutathione reductase, and catalase. Serum tumor necrosis factor-alpha (TNF-α) was decreased in the group treated with CCl(4) plus WGP (150 and 300 mg/kg bw). Histopathological examination of livers showed that WGP reduced fatty degeneration, cytoplasmic vacuolization and necrosis in CCl(4)-treated rats. In contrary, 10mg/kg bw of gallic acid was administrated, this dose was related with WGP (300 mg/kg bw), and had significantly decreased the AST and ALT compared to the CCl(4)-treated group. Aforesaid results suggested that gallic acid from WGP offered antioxidative activity against CCl(4)-induced oxidative liver damage. CONCLUSIONS Taken together, this study is the first time to suggest that Graptopetalum paraguayense E. Walther exerts hepatoprotection via promoting antioxidative and anti-inflammatory properties against CCl(4)-induced oxidative liver damage.

Ice plant (Mesembryanthemum crystallinum) improves hyperglycaemia and memory impairments in a Wistar rat model of streptozotocin-induced diabetes

BACKGROUND Ice plant (Mesembryanthemum crystallinum) has been used as an anti-diabetic agent in Japan because it contains d-pinitol. The efficacy of ice plant in the regulation of blood glucose is unclear at present. Recently, memory impairment and development of Alzheimers disease found in diabetic patients are thought to be caused by high blood glucose. The mechanism by which ice plant protects against the impairment of memory and learning abilities caused by high blood glucose remains unclear. The aim of this study was to evaluate the protection of ice plant water extracts (IPE) and D-pinitol against memory impairments in a Wistar rat model of streptozotocin (STZ)-induced diabetes. We hypothesised that IPE and D-pinitol could suppress blood glucose and elevate insulin sensitivity in these rats. RESULTS For memory evaluation, IPE and D-pinitol also improved the passive avoidance task and the working memory task. In addition, inhibition of acetylcholinesterase activity in hippocampus and cortex was found in this rat model administered IPE or D-pinitol. IPE and D-pinitol also markedly elevated superoxide dismutase activity against oxidative stress and reduced malondialdehyde production in hippocampus and cortex of the rats. CONCLUSION These findings indicated that IPE and D-pinitol possess beneficial effects for neural protection and memory ability in a rat model of diabetes.

Reduction of mutagenicity of the fumes from cooking oil by degumming treatment

Abstract The fume of cooking oil has been reported to increase the risk of respiratory tract cancer. The influence of a degumming treatment of peanut oil on the contents of mutagenic compounds in fumes from heated peanut oil was investigated. The results indicate that the peanut oil prepared from roasted peanut kernels which underwent degumming treatment had a lower free fatty acid (FFA) content and a higher smoke point, was more clear in color, and produced less fumes when heated at smoke point. Moreover, when compared to untreated peanut oil, the mutagenicity of oil fumes of degummed peanut oil toward Salmonella typhimurium TA98 and TA100 was reduced to 81% and 73% ( p trans-trans -2,4-decadienal ( t-t- 2,4-DDE), trans-trans -2,4-nonadienal ( t-t- 2,4-NDE), trans -2-decenal ( t- 2-DCA), and trans -2-undecenal ( t -2-UDA) in oil fumes of degummed peanut oils were drastically decreased ( p t-t -2,4-DDE. The results also indicate that the FFA content had a high linear correlation with mutagenicity ( r 2 =0.9978) and content of t-t- 2,4-DDE ( r 2 =0.7685). Moreover, there was a correlation ( r 2 =0.7816) between the content and the mutagenicity of t-t- 2,4-DDE. The decrease of FFA by degumming might explain the reduction of mutagenic alkenal compounds and mutagenicity of fumes from heated peanut oil.

Graptopetalum paraguayense and resveratrol ameliorates carboxymethyllysine (CML)-induced pancreas dysfunction and hyperglycemia.

Hyperglycemia is associated with advanced glycation end products (AGEs). Recently, AGEs were found to cause pancreatic damage, oxidative stress, and hyperglycemia through the AGE receptor. Carboxymethyllysine (CML) is an AGE but whether it induces pancreatic dysfunction remains unclear. Graptopetalum paraguayense, a vegetable consumed in Taiwan, has been used in folk medicine and is an antioxidant that protects against liver damage. We investigated the protective properties of G. paraguayense 95% ethanol extracts (GPEs) against CML-induced pancreatic damage. The results indicated that resveratrol, GPE, and gallic acid (the active compound of GPE) increased insulin synthesis via upregulation of pancreatic peroxisome proliferator activated-receptor-γ (PPARγ) and pancreatic-duodenal homeobox-1 (PDX-1) but inhibited the expression of CML-mediated CCAAT/enhancer binding protein-β (C/EBPβ), a negative regulator of insulin production. Moreover, resveratrol and GPE also strongly activated nuclear factor-erythroid 2-related factor 2 (Nrf2) to attenuate oxidative stress and improve insulin sensitivity in the liver and muscle of CML-injected C57BL/6 mice and resulted in reduced blood glucose levels. Taken together, these findings suggested that GPE and gallic acid could potentially be used as a food supplement to protect against pancreatic damage and the development of diabetes.

Actinidia callosa peel (kiwi fruit) ethanol extracts protected neural cells apoptosis induced by methylglyoxal through Nrf2 activation.

Abstract Context: Methylglyoxal (MG) is a reactive dicarbonyl compound generated as an intermediate of glycolysis during the physical glycation in the diabetic condition. MG itself has been commonly implicated in the development of diabetic neuropathy. Several active compounds in Actinidia callosa have been found to inhibit glycation and MG-protein reaction. Objective: This study investigated the protective effects of A. callosa (kiwi fruits) peel ethanol extracts (ACE) on MG-induced Neuro-2A cell apoptosis. Materials and methods: The Neuro-2A cells pre-treated by ACE (50–200 μg/mL) or allyl-isothiocyanate (AITC) (50 μM) for 6 h, in turn, the cells were treated with MG (250 μM) for 24 h. Results: ACE or AITC treatment markedly inhibited the generation of reactive oxygen species (ROS) and the elevation of caspase-3 and capase-9 levels induced by MG in Neuro-2A cells. ACE and AITC elevated Bcl2 and inhibited Bax expressions in MG-induced Neuro-2A cells. ACE elevated Nrf2 transcriptional activity and nuclear translocation in MG-induced Neuro-2A cells. Nrf2 down-stream molecules including HO-1 and GCL were elevated by ACE or AITC treatment in MG-induced Neuro-2A cells. The protective effects of ACE on MG-induced Neuro-2A apoptosis were attenuated while Nrf2 knockdown. Discussion and conclusion: We established the first evidence that ACE might contribute to the prevention of the development of diabetic neuropathy by blocking the MG-mediated intracellular glycation system.