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Objective: The increasing consumer awareness of food, which can provide health benefits and potentially aid disease prevention, has become the driving force of the functional food market. Accordingly, the aim of this study was to investigate the effects of chicken genotype on the macronutrient content, bioactive peptide content, and antioxidant capacity within different breast meat.Methods: In this experiment, three genotypes of chicken, Thai indigenous, black-boned, and broiler (control), were reared with commercial feed under the same conditions. Thirty chickens were slaughtered at typical market age and the breasts were separated from the carcass to determine macronutrient content using the AOAC method. The antioxidant capacities of the chicken breasts were evaluated by in vitro antioxidant assays and the protein pattern was investigated using gel electrophoresis. Carnosine and anserine, which have antioxidant properties in animal tissue, were determined using high performance liquid chromatography.Results: The results showed that breast meat from Thai indigenous chickens had a greater macronutrient content and higher antioxidant capacity compared with the other genotypes (p

The combination of natural products is an alternative approach to achieving chemopreventive potential. Accordingly, citrus hesperidin exhibits numerous biological activities, including anticarcinogenic activities, while the sesamin in sesame exhibits potent anticancer activities and lipid-lowering effects. We investigated the cancer chemopreventive effects of mixed sesame and orange seed extract (MSO) containing hesperidin and sesamin in diethylnitrosamine (DEN)-induced hepatocarcinogenesis. Rats were injected with DEN once a week for 3 weeks to induce hepatocarcinogenesis. Rats were fed with MSO and various compositions that included sesame extract (SE) and hesperidin. The 10-week administration of MSO more effectively inhibited the number and size of hepatic GST-P-positive foci than hesperidin in DEN-initiated rats. MSO and hesperidin decreased the number of PCNA-positive hepatocytes but increased the apoptotic cells in DEN-induced rats. Furthermore, MSO and its constituents suppressed hepatic triglyceride content concurrently along with the expression of fatty acid synthase. Although the 5-week administration of MSO or hesperidin did not alter hepatic, preneoplastic lesion formation in DEN-initiated rats, it alleviated DEN-induced hepatotoxicity. MSO and its applied compositions did not impact upon the cytochrome P450 system. In conclusion, sesame extract promoted the chemopreventive effect of hesperidin on DEN-induced early stage of hepatocarcinogenesis in rats. The inhibitory mechanisms are likely involved with the induction of cell apoptosis, suppression of cell proliferation and modulation of hepatic lipogenesis. This study may provide revelations in the development of alternative treatments against hepatocellular carcinoma.

Excessive consumption of a fat- and/or fructose-rich hypercaloric diet leads to metabolic syndromes. This study aimed to investigate the hepatoprotective effects of tetrahydrocurcumin (THC), an anti-oxidant metabolite of curcumin, in a hypercaloric diet-induced oxidative stress mouse model. Male ICR mice were fed a high-fat and high-fructose diet (HFFD) containing hydrogenated soybean oil (44.1% saturated fat and 0.2% trans-fatty acids) and a 20% fructose solution for 8 weeks. The HFFD induced hepatic injury through cytochrome P450 (CYP450)-induced oxidative stress, increased glucose tolerance, and increased CYP450 expression. THC attenuated oxidative stress in the HFFD mice by decreasing glucose tolerance, alanine aminotransferase and aspartate aminotransferase levels. In addition, THC suppressed HFFD-induced NADPH-CYP450 reductase activity, restored expression of anti-oxidative stress response related genes, and reduced ROS production by CYP2E1 and CYP3A11. Thus, THC is an excellent candidate for protection against HFFD-induced liver injury related to phase I biotransformation and anti-oxidation pathway.

This study aimed to evaluate the cancer chemopreventive activity of vanillic acid (VA) in diethylnitrosamine- and 1,2-dimethylhydrazine-induced liver and colon carcinogenesis in rats. VA did not induce the formation of hepatic glutathione S-transferase placental form (GST-P) positive foci and colonic aberrant crypt foci, demonstrating no carcinogenic activity. VA (75 mg kg−1 body weight) could significantly reduce the number and areas of hepatic GST-P positive foci when administered before carcinogen injections, but no such effect was seen when it was administered after carcinogen injection. No protection was seen in the colon when VA was treated before or after carcinogen injection. Immunohistochemical studies demonstrated the decreased expression of proliferating cell nuclear antigen and the induction of apoptosis. Mechanistic studies showed that VA significantly induced the expression of GSTA-5 and Nrf-2 genes, which are associated with the detoxification system. Likewise, the antiproliferative effect was noticed by the reduction of Cyclin D1 expression. The apoptotic activity may be due to the upregulation of Caspase-3 and Bad levels and downregulation of the Bcl-2 level. These data suggest that VA exhibited significant protection against diethylnitrosamine- and 1,2-dimethylhydrazine-induced hepatocarcinogenesis, which might be related to the induction of the detoxifying enzyme, the reduction of proliferation and the induction of apoptosis.

Red yeast (Sporidiobolus pararoseus), obtained from glycerol waste in the biodiesel process, has been used as a mycotoxin sorbent in some agricultural products. This study focused on the antigenotoxic effects of red yeast on aflatoxin B1 (AFB1)-induced mutagenesis, using a Salmonella mutation assay and a rat liver micronucleus test. Red yeast was sequentially extracted to obtain hexane, acetone, hot water, and residue fractions. Carbohydrates were mainly found in hot water extract (HWE), while proteins were observed in the residue fraction. The amount of lycopene in hexane extract (HE) was higher than the amount of β-carotene in HE. All red yeast extracts were not mutagenic in the Salmonella typhimurium strains TA98 and TA100 under the presence and absence of metabolic activation. Among the extracts obtained from red yeast, HE presented the strongest antimutagenicity against AFB1-induced mutagenesis in both strains, but HWE did not show any antimutagenicity. The oral administration of red yeast, HE, and HWE for 28 days was further investigated in rats. These extracts did not induce micronucleated hepatocytes. Furthermore, they modulated the activities of some detoxifying enzymes but did not alter the activities of various cytochrome P450 isozymes. Notably, they significantly decreased hepatic micronucleus formation in AFB1-initiated rats. HE altered the activity of hepatic glutathione-S-transferase but did not affect its protein expression. Taken together, the antigenotoxicity of red yeast against AFB1-induced mutagenesis might be partly due to the modulation of some detoxifying enzymes in AFB1 metabolism. β-Carotene and lycopene might be promising antigenotoxic compounds in red yeast.

Rice bran oil (RBO) comprises various nutrients and phytochemicals which exhibit several health benefits. There are no studies regarding the functional effects of different colours of RBO. This study was aimed to compare the constituents and antioxidant activities of white rice bran oil (WRBO) and coloured rice bran oil (CRBO). Each RBO showed similar free fatty acid profiles. However, greater amounts of vitamin E, phytosterols, carotenoids, and chlorophylls were found in CRBO, which had lower γ-oryzanol content than WRBO. Oxidative stress was induced in male mice by an overdose of acetaminophen (APAP) at 300 mg/kg body weight. The mice were then fed with RBO at the equivalent dose to 100 mg/kg body weight of γ-oryzanol three hours later and sacrificed six hours after APAP treatment. The administration of 100 mg γ-oryzanol equivalent in CRBO ameliorated APAP-induced hepatotoxicity in mice more strongly than 100 mg γ-oryzanol equivalent in WRBO, as evidenced by the significant reduction of serum ALT, hepatocellular necrosis, and hepatic lipid peroxidation. CRBO could improve xenobiotic-metabolizing and antioxidant enzyme activities, including glutathione S -transferase, superoxide dismutase, glutathione peroxidase, and glutathione reductase, and also increase mRNA expression of various antioxidant-responsive genes. Vitamin E, phytosterols, carotenoids, and chlorophyll might be the protective compounds in CRBO that alleviate APAP-induced hepatotoxicity through the interruption of APAP metabolism and the activation of antioxidant systems at both transcriptional and enzymatic levels. These findings might provide a protective role of CRBO on oxidative stress associated with several degenerative diseases.

This study investigated the cancer chemopreventive effects of an acidic methanol extract of purple rice husk on chemically induced carcinogenesis in rats. This purple rice husk extract (PRHE) had high polyphenol contents. Vanillic acid was a major phenolic compound in PRHE. Three major anthocyanins found in PRHE were malvidin-3-glucoside, peonidin-3-glucoside and cyanidin-3-glucoside. PRHE was not toxic and clastogenic in rats. The LD50 of PRHE was greater than 2000 mg kg&minus, 1 body weight (BW). The oral administration of 300 or 1000 mg kg&minus, 1 BW of PRHE for 28 days significantly decreased the number of micronucleated hepatocytes in diethylnitrosamine-initiated rats. The inhibitory mechanisms were associated with the reduction of cytochrome P450 2E1 expression and induction of some detoxifying enzymes in the liver. In addition, treatment with 500 mg kg&minus, 1 BW of PRHE for eight weeks did not induce preneoplastic lesions in the liver and colon. It significantly inhibited hepatic glutathione-S-transferase positive foci formation induced by diethylnitrosamine and 1,2-dimethylhydrazine by suppression of hepatocyte proliferation and induction of apoptosis. In conclusion, PRHE did not present toxicity, clastogenicity or carcinogenicity in rats. It exhibited cancer chemopreventive properties against chemically induced early stages rat hepatocarcinogenesis. Anthocyanins and vanillic acid might be candidate anticarcinogenic compounds in purple rice husk.

The most challenging part of liver cancer detection is finding it in the very early stages. It has been argued that liver preneoplasia is found at the very earliest stages of liver cancer. The presence of a lesion is closely related to the development of HCC. We report herein a new class of iron-based T1 MRI contrast agents which are nanoparticles of iron–tannic complexes (so-called Fe–TA NPs) that can be used for detecting liver preneoplasia. Preliminary assessment of their toxicity in healthy rats provides suitable imaging dose ranges with acceptable toxicity. In diethylnitrosamine (DEN) induced rats, it is shown that Fe–TA NPs are capable of enhancing MRI signals in rat livers having pre-neoplastic lesions within 60 minutes post-injection. The enhancement efficacy is strongly dependent on the characteristics of pre-neoplastic foci (GST-P+ foci). The highest enhancement was in good correlation with the size of GST-P+ foci and amount of Fe–TA NPs accumulated in the liver, and might be caused by the dysfunction of liver sinusoids along with cellular uptake capability of pre-neoplastic hepatocytes. Our results show that Fe–TA NPs are of great interest to develop as an efficient MRI imaging agent for risk assessment of liver cancer.

The taste-active and nutritional components of Thai native, broilers, black-boned, and spent hen chickens were analyzed. The amounts of tasty amino acids especially glutamic acid were the highest in Thai native chicken. The black-boned chicken had the highest arginine content, related to the least amount of consumer satisfaction. Concerning nutritional quality, choline, and taurine were deemed important for brain function. The black-boned chicken showed the highest choline and taurine contents, unlike that of the spent hens. In contrast, broilers presented the highest betaine content, which might be attributed to their lipid metabolism. L-carnitine content was abundant in black-boned and Thai native chickens. Moreover, the amounts of essential amino acids were high in Thai native chicken. In conclusion, black-boned chicken proved to be an excellent nutritional source for health-conscience consumers, whereas the Thai native chickens were flavourful and delicious.

Background Cleistocalyx nervosum var. paniala is a local fruit mainly cultivated in the north of Thailand. Our previous study has reported that the methanol extract of C. nervosum seed presented antimutagenicity in a Salmonella mutation assay. The present study focused on the effect of a low-polar extract of C. nervosum seed on the early stages of diethylnitrosamine (DEN)- and dimethylhydrazine (DMH)-induced carcinogenesis in rats. Methods Dried C. nervosum seed powder was extracted using dichloromethane. To study its effect on the initiation stage of carcinogenesis of rats, they were fed with various doses of C. nervosum seed extract (CSE) for 21 days. DEN injection was used to initiate hepatocarcinogenesis and partial hepatectomy was performed to amplify mutated hepatocytes resulting in micronucleated hepatocyte formation. To study the role of CSE on the promotion stage, rats were injected with DEN and DMH to induce preneoplastic lesions and the numbers of glutathione S-transferase placental form (GST-P) positive foci in the liver and aberrant crypt foci (ACF) in the colon were measured. This was followed by CSE administration for 10 weeks. The inhibitory mechanisms of CSE on initiation and promotion stages, including xenobiotic metabolism, cell proliferation and apoptosis, were investigated. Results The total phenolic content in CSE was 80.34 ± 2.29 mg gallic acid equivalents (GAE) per g of extract and 2,4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone was found to be a major flavonoid. The main terpenoids in CSE were β-selinene, α-selinene, γ-selinene and o-cymene while 24(Z)-methyl-25-homocholesterol was a major phytosterol. CSE significantly decreased the number of micronucleated hepatocytes in DEN-initiated rats and enhanced the activities of hepatic glutathione S-transferase and UDP-glucuronyltransferase. Furthermore, the formation of preneoplastic lesions in the liver and colon was statistically reduced by CSE. CSE also diminished cell proliferation in the liver and colon indicated by the number of PCNA positive cells. However, CSE did not alter the numbers of apoptotic hepatocytes and colonocytes in DEN- and DMH-initiated rats. Conclusions The dichloromethane extract of C. nervosum seed demonstrated chemopreventive effects on chemically-induced carcinogenesis in both initiation and promotion stages in rats. The inhibitory mechanism might be involved in the modulation of hepatic detoxifying enzymes and suppression of hepatocyte and colonocyte proliferation.

Diethylnitrosamine (DEN) and 1,2-dimethylhydrazine (DMH) are classical carcinogens used in experimental rodent carcinogenesis. However, the interaction effects of these carcinogens on biochemical and molecular changes during carcinogenesis have not been investigated. Therefore, the effect of DEN and DMH co-administration on preneoplastic lesion formation and its molecular mechanism in rats were determined. Triple intraperitoneal administrations of DEN were made before, during or after double subcutaneous injections of DMH. At week 8 of the experiment, the preneoplastic hepatic glutathione

This study aimed to investigate the effect of low intensity of high pressure processing (LHP) on bioactive compound content and the antioxidant capacity of persimmon before digestion and during simulated in vitro gastrointestinal digestion (IVD). The astringent and non-astringent persimmon cultivars treated with LHP at 100 MPa for 10 min were analyzed for polyphenols, antioxidant activities and bioaccessibility. The results showed that LHP treatment significantly increased (P

Background Rice husk, a waste material produced during milling, contains numerous phytochemicals that may be sources of cancer chemopreventive agents. Various biological activities of white and colored rice husk have been reported. However, there are few comparative studies of the cancer chemopreventive effects of white and colored rice husk. Methods This study investigated the cancer chemopreventive activities of two different colors of rice husk using in vitro and in vivo models. A bacterial mutation assay using Salmonella typhimurium strains TA98 and TA100 was performed; enzyme induction activity in murine hepatoma cells was measured, and a liver micronucleus test was performed in male Wistar rats. Results The white rice husk (WRHE) and purple rice husk (PRHE) extracts were not mutagenic in Salmonella typhimurium TA98 or TA100 in the presence or absence of metabolic activation. However, the extracts exhibited antimutagenicity against aflatoxin B1 (AFB1) and 2-amino-3,4 dimethylimidazo[4,5-f]quinolone (MeIQ) in a Salmonella mutation assay. The extracts also induced anticarcinogenic enzyme activity in a murine Hepa1c1c7 hepatoma cell line. Interestingly, PRHE but not WRHE exhibited antigenotoxicity in the rat liver micronucleus test. PRHE significantly decreased the number of micronucleated hepatocytes in AFB1-initiated rats. PRHE contained higher amounts of phenolic compounds and vitamin E than WRHE in both tocopherols and tocotrienols as well as polyphenol such as cyanidin-3-glucoside, protocatechuic acid and vanillic acid. Furthermore, PRHE increased CYP1A1 and 1A2 activities while decreasing CYP3A2 activity in the livers of AFB1-treated rats. PRHE also enhanced various detoxifying enzyme activities, including glutathione S-transferase, NAD(P)H quinone oxidoreductase and heme oxygenase. Conclusions PRHE showed potent cancer chemopreventive activity in a rat liver micronucleus assay through modulation of phase I and II xenobiotic metabolizing enzymes involved in AFB1 metabolism. Vitamin E and phenolic compounds may be candidate antimutagens in purple rice husk. Electronic supplementary material The online version of this article (10.1186/s12906-019-2647-9) contains supplementary material, which is available to authorized users.

This study aims to determine the anti-carcinogenic effects of the proanthocyanidin-rich fraction (PRFR) obtained from red rice germ and bran extract on HepG2 cells. The PRFR obtained from red rice germ and bran extract could reduce the cell viability of HepG2 cells as shown by the IC50 value at 20 &micro, g/mL. Notably, PRFR concentrations at 20 and 40 &micro, g/mL significantly increased the number of cells in the G2/M phase from 25.7% &plusmn, 1.4%in the control group to 36.2% &plusmn, 3.4% (p &lt, 0.01) and 48.9% &plusmn, 2.6% (p &lt, 0.0001), respectively, suggesting that the cells were arrested in this phase, which was confirmed by the reduction of survival proteins, including cyclin B1 and cdc25. Moreover, the PRFR at 20 and 40 &micro, g/mL could induce cell death via the apoptosis cascade, indicated by the percentage of total apoptotic cells from 9.9% &plusmn, 3.1% in the control group to 41.1 &plusmn, 3.9 (p &lt, 0.0001) and 82.2% &plusmn, 5.8% (p &lt, 0.0001), respectively. This was clarified by increasing apoptotic proteins (such as cleaved PARP-1, cleaved caspase-8 and cleaved caspase-3) and decreasing anti-apoptotic protein survivin without p53 alterations. These results demonstrated that the PRFR obtained from red rice germ and bran extract could inhibit cell proliferation and induce cell apoptosis in HepG2 cells via survivin, which could potentially serve as a new target for cancer therapeutics making it an excellent &ldquo, lead candidate&rdquo, molecule for in vivo proof-of concept studies.

In this study, corncob xylooligosaccharides (corncob-XOS) were prepared enzymatically, and their beneficial effects, compared to commercial prebiotics, including fructooligosaccharides (FOS), gentiooligosaccharides (GTO), inulin, isomaltooligosaccharides (IMO), lactulose, and commercial xylooligosaccharides (commercial-XOS), were assessed. The prebiotic property of corncob-XOS, in which they enhance the growth of probiotic lactic acid bacteria (LAB), namely Lactobacillus casei TISTR1463, L. delbrueckii subsp. lactis TISTR1464, and L. plantarum TISTR1465, was tested. The result revealed that this prebiotic is a good carbon source due to its ability to promote growth and induce β-xylosidase production in all tested strains. Corncob-XOS showed excellent 2,2′-diphenyl-1-picryl-hydrazyl (DPPH) and 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activities as well as ferric reducing antioxidant power (FRAP), and the total phenolic compound content was remarkably high. The in vivo acute oral toxicity of corncob-XOS, based on behavioral alterations and the mortality of rats, was investigated. There was no significant toxic effect on body weight (bw), vital organ weight, or essential parameters of blood at the single dose level of 5000 mg/kg bw at p > 0.05. Furthermore, the median lethal dose (LD50) of corncob-XOS suggests that they are non-toxic. Taken together, these results support the further application of corncob-XOS as alternative forms of functional foods.

Ulcerative colitis (UC) results from colonic epithelial barrier defects and impaired mucosal immune responses. In this study, we aimed to investigate the modifying effects of a Spirogyra neglecta extract (SNE), a polysaccharide extract (PE) and a chloroform fraction (CF) on dextran sodium sulfate (DSS)-induced colitis in mice and to determine the mechanisms. To induce colitis, ICR mice received 3% DSS in their drinking water for 7 days. Seven days preceding the DSS treatment, oral administration of SNE, PE and CF at doses of 50, 25 and 0.25 mg/kg body weight (low dose), 200, 100 and 1 mg/kg body weight (high dose) and vehicle was started and continued for 14 days. Histologic findings showed that DSS-induced damage of colonic epithelial structure and inflammation was attenuated in mice pre-treated with SNE, PE and CF. Furthermore, SNE and PE significantly protected colonic epithelial cells from DSS-induced cell cycle arrest, while SNE, PE and CF significantly diminished apoptosis. Proteome analysis demonstrated that SNE and PE might ameliorate DSS-induced colitis by inducing antioxidant enzymes, restoring impaired mitochondria function, and regulating inflammatory cytokines, proliferation and apoptosis. These results suggest that SNE and PE could prevent DSS-induced colitis in ICR mice by protection against and/or aiding recovery from damage to the colonic epithelium, reducing ROS and maintaining normal mitochondrial function and apoptosis.

Replicative senescence, which is caused by telomere shortening from the end replication problem, is considered one of the tumor-suppressor mechanisms in eukaryotes. However, most cancers escape this replicative senescence by reactivating telomerase, an enzyme that extends the 3'-ends of the telomeres. Previously, we reported the telomerase inhibitory effect of a crude Zingiber officinale extract (ZOE), which suppressed hTERT expression, leading to a reduction in hTERT protein and telomerase activity in A549 lung cancer cells. In the present study, we found that ZOE-induced telomere shortening and cellular senescence during the period of 60 days when these A549 cells were treated with subcytotoxic doses of ZOE. Using assay-guided fractionation and gas chromatography/mass spectrometry analysis, we found that the major compounds in the active subfractions were paradols and shogaols of various chain lengths. The results from studies of pure 6-paradol and 6-shogaol confirmed that these two compounds could suppress hTERT expression as well as telomerase activity in A549 cells. These results suggest that these paradols and shogaols are likely the active compounds in ZOE that suppress hTERT expression and telomerase activity in these cells. Furthermore, ZOE was found to be nontoxic and had an anticlastogenic effect against diethylnitrosamine-induced liver micronucleus formation in rats. These findings suggest that ginger extract can potentially be useful in dietary cancer prevention.

Purpose: To study the effect of Cleistocalyx nervosum extract (CE) on diethylnitrosamine (DEN) and phenobarbital (PB) induced oxidative stress in early stages of rat hepatocarcinogenesis. Materials and Methods: Male Wistar rats were divided into 4 groups, with Group 1 as a negative control and Group 2 was a positive control receiving DEN injections once a week and PB in drinking water for 6 weeks. Two weeks before DEN initiation and PB treatment, Groups 3 and 4, were fed with 500 and 1000 mg/kg of CEs, respectively, for 8 weeks. Results: A number of GST-P-positive foci, preneoplastic lesions, in the liver were markedly increased in carcinogen administered rats, but was comparatively decreased in rats treated with 1000 mg/kg of CE. The CE reduced malondialdehyde in serum and in the livers of rats treated with DEN and PB. Moreover, CE significantly increased the activities of glutathione peroxidase and catalase in rat liver. Conclusions: CE appeared to exert its chemopreventive effects by modulating antioxidant status during DEN and PB induced early stages of hepatocarcinogenesis in rats.

This study focused on the chemopreventive effects of Spirogyra neglecta extract (SNE) and dried S. neglecta mixed diet on the early stages of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats. Male Wistar rats were injected with DMH to initiate aberrant crypt foci (ACF) formation. In the initiation stage, SNE significantly decreased the number of ACF in the colon of DMH-treated rats. Rats that received a low dose of SNE showed enhanced activity of several detoxifying and antioxidant enzymes. In the postinitiation stage, a low dose of SNE significantly decreased the number of ACF in the colon of DMH-treated rats. It significantly reduced the number of proliferating cell nuclear antigen-positive cells and increased the number of apoptotic cells in colonic crypts. S. neglecta thus inhibited the development of the early stages of DMH-induced colon carcinogenesis in rats by modulation of xenobiotic metabolizing enzymes and inhibition of cell proliferation as well as induction of apoptosis.

Use of natural products is one strategy to lessen cancer incidence. Rice bran, especially from colored rice, contains high antioxidant activity. Cancer chemopreventive effects of hydrophilic purple rice bran extract (PRBE) and white rice bran extract (WRBE) on carcinogen-induced preneoplastic lesion formation in livers of rats were investigated. A 15-week administration of PRBE and WRBE did not induce hepatic glutathione S-transferase placental form (GST-P) positive foci formation as the biomarker of rat hepatocarcinogenesis. PRBE and WRBE at 500 mg/kg body weight significantly decreased number and size of GST-P positive foci in diethylnitrosamine (DEN)-initiated rats. The number of proliferating nuclear antigen positive hepatocytes were also reduced in preneoplastic lesions in both PRBE and WRBE fed DEN-treated rats. Notably, the inhibitory effect on GST-P positive foci formation induced by DEN during the initiation stage was found only in rats treated by PRBE for five weeks. Furthermore, PRBE attenuated the expression of proinflammatory cytokines involving genes including TNF-&alpha, iNOS, and NF-&kappa, B. PBRE contained a higher number of anthocyanins and other phenolic compounds and vitamin E. PRBE might protect DEN-induced hepatocarcinogenesis in rats via attenuation of cellular inflammation and cell proliferation. Anthocyanins and other phenolic compounds, as well as vitamin E, might play a role in cancer chemopreventive activity in rice bran extract.

Free radicals are one of the causes of chronic and degenerative diseases. Antioxidants can protect the progression of free radical mediated disorders. The aim of this study was to evaluate the antioxidant activity of Spirogyra neglecta (Hassall) Kützing in rats. The rats were divided into 5 groups. Group 1 served as control. Groups 2 and 3 were administered hot water extract of S. neglecta at 50 and 200 mg/kg bw, respectively, while groups 4 and 5 were fed 1% and 4% S. neglecta mixed diet, resp., for 13 weeks. Antioxidant enzymes were evaluated in livers of the rats. The activities of catalase and glutathione reductase were significantly increased in the group fed 50 mg/kg of the extract, compared with the control group. Glutathione peroxidase activity was also significantly higher in the group fed 50 and 200 mg/kg of the extract. The study suggests that S. neglecta may enhance antioxidant systems in the rat liver.

Pinocembrin (5, 7-dihydroxyflavanone) is a flavanone extracted from the rhizome of Boesenbergia pandurata. Our previous studies demonstrated that pinocembrin had no toxicity or mutagenicity in rats. We here evaluated its effects on the initiation and promotion stages in diethylnitrosamine-induced rat hepatocarcinogenesis, using short- and medium-term carcinogenicity tests. Micronucleated hepatocytes and liver glutathione-S-transferase placental form foci were used as end point markers. Pinocembrin was neither mutagenic nor carcinogenic in rat liver, and neither inhibited nor prevented micronucleus formation as well as GST-P positive foci formation induced by diethylnitrosamine. Interestingly, pinocembrin slightly increased the number of GST-P positive foci when given prior to diethylnitrosamine injection.

Clesitocalyx nervosum var. paniala, an edible fruit found in some parts of Southeast Asia including Thailand, contains high amounts of polyphenols and has multiple biological activities. The purposes of this study were to evaluate the genotoxic and antigenotoxic effects of methanol extracts of C. nervosum seeds via a Salmonella mutation assay and a rat liver micronucleus test. C. nervosum extract was not mutagenic to Salmonella typhimurium strains TA98 and TA100 in both the presence and absence of metabolic activation. Furthermore, C. nervosum seed extract presented antigenotoxicity against aflatoxin B1, MeIQ and AF-2 induced mutagenesis. Clastogenicity and anticlastogenicity of C. nervosum seed extracts were determined in rat livers. Male wistar rats were divided into 6 groups. Groups 1 and 3 were treated with 5% tween-80 as a vehicle control. Group 2 received 1,000 mg/kg bw of methanol seed extract and groups 4–6 were fed with 20, 100 and 1,000 mg/kg bw of seed extracts, respectively for 21 days. At day 15 and 18 of the experiment, treated rats in groups 3–6 were intraperitoneally injected with 30 mg/kg bw of diethylnitrosamine to initiate hepatocarcinogenesis. At day 22, all rats were partially hepatectomized to amplify mutated hepatocytes. C. nervosum seed extract did not affect micronucleus formation in rat livers, but did slightly decrease the frequencies of micronucleated hepatocytes of diethylnitrosamine treated rats. In conclusion, the methanol extract of C. nervosum seed may contain chemopreventive compounds against carcinogenesis.

We designed an open-label, randomized two-phase crossover study to investigate the antioxidant effects after single and multiple doses of a coffee enema versus coffee consumed orally. Eleven healthy subjects were randomly assigned to either receive a coffee enema (3 times weekly for 6 visits) or consume ready-to-drink coffee (2 times daily for 11 days). After a washout period, subjects were switched to receive the alternate coffee procedure. Blood samples were collected at specific time points for the determination of serum levels of glutathione (GSH), malondialdehyde (MDA) and trolox equivalent antioxidant capacity (TEAC). The findings showed that either single or multiple administrations of the coffee enema or orally consumed coffee doses seemed not to produce any beneficial effects to enhance serum GSH levels or to decrease serum MDA levels over the study period of 12 days. In contrast, mean serum TEAC levels at day 12 after the coffee enema and at days 6 and 12 after oral coffee consumption were significantly reduced from their corresponding baseline values. Thus, no beneficial effects with respect to an enhancement of serum GSH and TEAC levels or a decrease in serum MDA concentrations were demonstrated after coffee enema or orally consumed ready-to-drink coffee.

Kojic acid (KA), a naturally occurring compound, is contained in traditional Japanese fermented foods and is used as a food additive, preservative and a dermatological skin-lightening agent. In the present experiment, initiation (experiment 1) and promotion (experiment 2) effects of KA-induced hepatocarcinogenesis were studied by rat medium-term bioassay for carcinogenicity. Male F344 rats were administered a diet containing 0-2% KA. Experiment 1 demonstrated that KA had no effect on induction of liver preneoplastic lesions or glutathione S-transferase placental form (GST-P) positive foci, in either number or area. In experiment 2, 2% KA treatment significantly increased the number and area of GST-P positive foci, but concentrations less than 0.5% did not. Moreover, 2% KA treatment significantly increased 8-OHdG levels and PCNA positive hepatocytes. The results indicated that low concentrations of KA do not have initiation effects on rat hepatocarcinogenesis, while higher concentrations of KA do promote hepatocarcinogenesis in rats. Thus, the results indicate that KA is a non-genotoxic hepatocarcinogen, showing the possible existence of a perfect threshold.

Pinocembrin, 5, 7 – dihydroxyflavanone, is one of the flavanones found in the rhizomes of Boesenbergia pandurata. Previous study demonstrated that pinocembrin was neither toxic nor mutagenic to male rats. This study evaluated the effects of pinocembrin on phase I and II xenobiotic-metabolizing enzymes in rat liver. It was found that heme oxygenase activity significantly increased in 10 and 100 mg/kg bw of pinocembrin treated groups (p < 0.05). However, pinocembrin did not affect the activities of NADPH: cytochrome P450 reductase, NADPH: quinone reductase, UDPglucuronosyltransferase and glutathione-S-transferase. It also did not affect the expression of phase I metabolizing enzymes, including CYP1A1, CYP2B1, CYP2C11, CYP2E1, CYP3A2, and NADPH: cytochrome P450 reductase. In conclusion, short-term treatment of pinocembrin in Wistar rats increased the activity of heme oxygenase but did not affect on the activities of other phase II xenobiotic-metabolizing enzymes or the expression of cytochrome P450 enzymes.

Pigmented rice bran has been suggested to be a valuable source of beneficial phytochemicals. We investigated genotoxic and anti-genotoxic effects of purple rice bran extract (PRBE) in rats using a liver micronucleus assay. Purple rice bran was extracted with methanol, obtaining large amounts of phenolic compounds, including anthocyanins and small amounts of gamma-oryzanol. The experimental protocols were divided into two sets. Male rats were divided into three groups. Group 1 was a negative control, while Groups 2 and 3 were fed with 100 and 500 mg/kg bw of PRBE, respectively, for 28 days. PRBE had no effect on micronucleus formation or xenobiotic metabolizing enzymes in rat liver. Experiments concerning the effect of PRBE on AFB1 showed that PRBE significantly lessened the amount of micronucleated hepatocytes in AFB1 treated rats. Furthermore, it modulated metabolic activation of AFB1 metabolism in the liver by suppressing activity and protein expression of CYP1A2, CYP3A and CYP 450 reductase, and enhancing phase II enzymes including GST and UGT. Overall, purple rice bran extract was not genotoxic in rats. It exhibited anti-genotoxicity by modulation some xenobiotic enzymes active in AFB1 metabolism.

Purple rice (Oryza sativa L. var. indica) cv. Kum Doisaket is cultivated in northern Thailand. This study evaluated the mutagenic and antimutagenic properties of hydrophilic and lipophilic components of purple rice using the Ames test. The seed and hull of purple rice were extracted with hexane, methanol, ethanol, and water. The methanol extracts had the highest amounts of phenolic acids and flavonoids, while the hexane extracts contained large amount of tocols and γ-oryzanol. None of the extracts were mutagenic in Salmonella typhimurium strains TA98 and TA100. The hexane extract of rice hull and the methanol extract of rice seed were strongly effective against aflatoxin B1- and 2-amino-3, 4 dimethylimidazo (4, 5-f) quinoline-induced mutagenesis, while aqueous extracts showed weakly antimutagenic properties. All extracts with the exception of aqueous extracts enhanced the number of revertant colonies from benzo (a) pyrene induced-mutagenesis. None of the extracts inhibited mutagenesis induced by the direct mutagens 2-(2-furyl)-3-(5-nitro-2-furyl)-acrylamide and sodium azide. The hull extracts showed more potent antimutagenicity than the seed extracts. Based on a chemical analysis, γ-oryzanol and γ-tocotrienol in the hull and cyanidin-3-glucoside and peonidin-3-glucoside in the seed are candidate antimutagens in purple rice. The antimutagenic mechanisms of purple rice might be related to either modulation of mutagen metabolizing enzymes or direct attack on electrophiles. These findings supported the use of Thai purple rice as a cancer chemopreventive agent.

Previous experiments showed that treatment of mice and rats with thioacetamide (TAA) induced liver cell damage, fibrosis and/or cirrhosis, associated with increased oxidative stress and activation of hepatic stellate cells. Some experiments suggest that CYP2E1 may be involved in the metabolic activation of TAA. However, there is no direct evidence on the role of CYP2E1 in TAA-mediated hepatotoxicity. To clarify this, TAA-induced hepatotoxicity was investigated using Cyp2e1-null mice. Male wild-type and Cyp2e1-null mice were treated with TAA (200 mg/kg of body weight, single, i.p.) at 6 weeks of age, and hepatotoxicity examined 24 and 48 h after TAA treatment. Relative liver weights of Cyp2e1-null mice were significantly different at 24 h compared to wild-type mice (p