<p>OBJECTIVETo investigate the association of the NAD(P)H: quinone oxidoreductase 1 (NQO1) C609T polymorphism with susceptibility to esophageal squamous cell carcinoma (ESCC) in a northern Chinese population.p><p>METHODSThe NQO1 C609T genotypes were determined by polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) analysis in 193 patients with ESCC and 141 unrelated healthy controls.p><p>RESULTSThe frequency of the T allele (null) among ESCC patients was significantly higher than that among healthy controls (Chi-square=4.86, P=0.028). The NQO1 C/C and C/T genotype distribution among ESCC patients was not significantly different from that among healthy controls (Chi-square= 2.27 and 0.127; P=0.132 and 0.721, respectively). However, the T/T genotype frequency among ESCC patients was significantly higher than that among healthy controls (Chi-square=4.39, P=0.036). The NQO1 T/T genotype significantly increased the risk for developing ESCC, compared to the combination of C/C and C/T genotypes, with the adjusted odds ratio (OR) of 1.81 (95%CI: 1.04-3.15). This increased susceptibility exhibited pronouncedly in patients with family history of upper gastrointestinal cancers (adjusted OR=2.22, 95%CI 1.18-4.17).p><p>CONCLUSIONDetermination of the NQO1 C609T genotype may be used as a stratification marker to predicate high-risk individuals for ESCC.p>
Esophageal Neoplasms ; genetics ; Genetic Predisposition to Disease ; Genotype ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Polymorphism, Genetic

We investigated the growth inhibitory effects of Atrina pecitinata (AP) on the proliferation in human cancer cell lines in vitro. AP was extracted with methanol which was further fractionated into four diffferent types: methanol (APMM), haxane (APMH), butanol (APMB), and aquous layers (APMA). Among various partition layers, the APMM showed the strongest cytotoxic effects on all cancer cell lines which we used. In the MTT assay of AP fractions, the growth inhibitory effects was increased in proportion to its concentration. We observed quinone reductase (QR) induced effects in all fraction layers of AP on HepG2 cells. The QR induced effects of APMM on HepG2 cell at 80 microgram/mL concentration indicated 2.0 with a control value of 1.0.
Cell Line* ; Hep G2 Cells ; Humans ; Methanol ; NAD(P)H Dehydrogenase (Quinone)

In this study, we investigated antimicrobial and cytotoxicity effects to each fraction extracted from Hizikia fusiformis (HF), which were extracted methanol (HFM)and then the extract was fractionated into four different types: hexane (HFMH), methanol (HFMM), butanol (HFMB) and aquous (HFMA) partition layers. We determined the cytotoxic effect of these layers on human cancer cells by MTT assay. Among various partition layers of HF, the HFMB and HFMM were showed the strong cytotoxic effects on cancer cell lines we used. The quinone reductase (QR) induced activity of the HFMB on HepG2 cells at 150 microgram/mL concentration was 2.63 times more effective compared to the control value of 1.0. Although further studies are needed, the present work suggests that HF maybe a chemopreventive agent for the treatment of human cancer cells.
Cell Line ; Hep G2 Cells ; Humans ; Methanol ; NAD(P)H Dehydrogenase (Quinone)

Esophageal Neoplasms ; genetics ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Point Mutation ; Polymorphism, Genetic

In this study, we investigated the anticancer activity of the fin of Thunnus Thynnus (TT ). TT was extracted with methanol (TTM ), and then further fractionated into four subfractions by using solvent partition method, affording hexane (TTMH ), methanol (TTMM ), butanol (TTMB )and aquous (TTMA )soluble fractions. We determined the cyto-toxicity of these four fractions in four kind of cancer cell lines, such as HepG2, MCF-7, B16-F10 and HT29 by MTT assay. The TTMM showed the strongest cytotoxic effect at the concentration of 150 microgram/mL, displaying 95% on the HepG2 cell lines and 82% on MCF-7 cell line. The morphological changes such as membrane shirinking and blebbing of cells were also observed by TTMM treatment in HT29 cell. In addition, we observed that quinone reductase (QR ) activity was elevated by only TTMM and TTMH treatments in HepG2 cell. QR activity was increased to around 2.0 and 1.8 times in TTMM and TTMH treated HepG2 cell at 100 microgram/mL, respectively, compared to that in control. Although further studies are needed, the present work could suggest that the fin of TT has a potential to be usable as a chemo-preventive agent against cancer.
Blister ; Cell Line ; Hep G2 Cells ; HT29 Cells ; Humans ; MCF-7 Cells ; Membranes ; Methanol ; NAD(P)H Dehydrogenase (Quinone)*

PURPOSE: Two types of chitosan oligosaccharides (COSs), COS I and COS II, were investigated for the effects on ascitic tumor and enzymes for cancer chemoprevention. MATERIALS AND METHODS: Chitosan oligosaccharides were administered once daily for 10 days after the tumor implantation. The change of body weight was observed for 20 days, and the survival rate of mice was determined after 21 days. Chitosan oligosaccharides were administered once daily for 10 days before the tumor implantation (1 106 cells). The number of ascitic tumor cells were measured at 6 days after tumor implantation. Chemopreventive potential of chitosan oligosaccharides was examined by the induction of quinone reductase and inhibition of cytochrome P450 1A1. RESULTS: Chitosan oligosaccharides exerted antitumor activity by inhibiting the growth of Ehrlich ascites tumor cells in vivo. Mice given Ehrlich cells and 10 or 100 mg/kg body weight of chitosan oligosaccharides had 33% survival after 21 days. Quinone reductase activity was increased with chitosan oligosaccharides. There were 26% and 33% inhibition in the activity of cytochrome P450 1A1 enzyme with the treatment of COS I and COS II, respectively. CONCLUSION: These results suggest that chitosan oligosaccharides has antitumor activity and cancer chemo preventive potential by inducing QR activity and inhibiting cytochrome P450 1A1.
Animals ; Body Weight ; Carcinoma, Ehrlich Tumor ; Chemoprevention* ; Chitosan* ; Cytochrome P-450 Enzyme System ; Mice ; NAD(P)H Dehydrogenase (Quinone) ; Oligosaccharides ; Survival Rate

Carcinoma, Medullary ; metabolism ; Carcinoma, Neuroendocrine ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; metabolism ; NADP ; metabolism ; Neoplasm Proteins ; metabolism ; Prognosis ; Thyroid Neoplasms ; metabolism

<p>OBJECTIVETo explore the relationship between quinone oxidoreductase1 (NQO1) gene nonsynonymous cSNP and the genetic susceptibility of esophageal cancer.p><p>METHODSPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and Allele-Specific PCR (AS-PCR) were employed to assess the polymorphism of NQO1 genes both in 106 patients with esophageal cancer and control subjects matched by age, gender and origin.p><p>RESULTSIt was shown that no C/C genotype was found at 406 of NQO1. The allelic frequency of NQO1 609T was significantly higher in patients with esophageal cancer than in the control subjects (P < 0.005) and the individuals with 609T allelic genotype of NQO1 gene were at greater risk to develop esophageal cancer (OR = 4.76, 95% CI = 1.064 - 3.397). But Individuals with mutant allele of NQO1 465 genotype did not show the rising risk of esophageal cancer.p><p>CONCLUSIONSThe NQO1 C609T polymorphisms should likely be associated with the genetic susceptibility of esophageal cancer.p>
Alleles ; China ; Esophageal Neoplasms ; ethnology ; genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Polymorphism, Single Nucleotide

<p>OBJECTIVETo explore the relationship between genetic polymorphism of quinone oxidoreductase 1 (NQO1), glutathione S-transferase theta 1 (GSTT1), glutathiones S-transferase mu 1 (GSTM1) and susceptibility to chronic benzene poisoning (BP).p><p>METHODSThe genotypes of NQO1, GSTT1, GSTM1 for 100 patients with benzene poisoning and 90 workers exposed to benzene who were engaged in the same working time and job title as patients with benzene poisoning were detected by PCR-RFLP and multi-PCR.p><p>RESULTSThere was a 2.82-fold (95% CI: 1.42 approximately 5.58, P < 0.05) increased risk of BP in the subjects with NQO1 C609T mutation genotype (T/T) compared with those carrying heterozygous (C/T) and wild type (C/C), and there was a 2.94-fold (95% CI: 1.25 approximately 6.90, P < 0.05) increased risk of BP in the subjects with NQO1 C609T T/T genotype compared with those carrying C/C genotype. The subjects with GSTT1 null genotype had a 1.91-fold (95% CI: 1.05 approximately 3.45, P < 0.05) increased risk of BP compared with those with GSTT1 non-null genotype. The interaction of two genes showed that there was a increased risk of BP in subjects with any two genotypes of NQO1 C609T T/T genotype and GSTT1 null genotype and GSTM1 null genotype, compared to the individual with any two genotypes of NQO1 C609T C/C genotype and GSTT1 non-null genotype and GSTM1 non-null genotype. The interaction of three genes showed that there was a 20.41-fold (95% CI: 3.79 approximately 111.11, P < 0.01) increased risk of BP in subjects with NQO1 C609T T/T genotype and GSTT1 null genotype and GSTM1 null genotype compared with those carrying NQO1 C609T C/T genotype and C/C genotype and GSTT1 non-null genotype and GSTM1 non-null genotype.p><p>CONCLUSIONSThe interaction of multi-genes may be an important role to BP. The genetic polymorphisms of 3 genes (NQO1, GSTT1 and GSTM1) led to declining of detoxifying ability in benzene metabolism, so the individual with NQO1 C609T T/T genotype, GSTT1 null genotype and GSTM1 null genotype is most susceptive to benzene. The results were consistent with that of the theoretic presumption. It could be suggested as a biomarker to assess the risk of benzene poisoning for individuals.p>
Adult ; Aged ; Benzene ; poisoning ; Case-Control Studies ; Chronic Disease ; Female ; Genetic Predisposition to Disease ; Glutathione Transferase ; genetics ; Humans ; Male ; Middle Aged ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Polymorphism, Genetic

<p>OBJECTIVETo investigate the association between the C609T polymorphism of NADP (H): quinoneoxidoreductase 1 (NQ01) gene and decreased cognitive function and sporadic Alzheimer's disease (AD) in a community cohort.p><p>METHODSPolymerase chain reaction (PCR), denaturing high performance liquid chromatography (DHPLC) and sequencing were used to determine the genotype of NQ01 in 110 subjects without cognitive dysfunction, 21 with cognitive dysfunction, and 65 AD patients from a community cohort.p><p>RESULTSSignificantly different distributions of C/T and T/T genotypes were found between MMSE normal and abnormal subjects (OR=2.8, 95%CI 0.96-8.18, P=0.024), and between AD patients and healthy controls (OR=3.27, 95% CI 1.54-6.94, P=0.001), respectively. The frequencies of T allele of NQ01 C609T were significantly higher in MMSE abnormal subjects and AD patients (P=0.034 and 0.005) as compared to normal controls.p><p>CONCLUSIONThe C609T polymorphism of NQ01 gene may be a genetic risk factor for cognitive dysfunction and sporadic AD in Chinese population.p>
Alzheimer Disease ; genetics ; Base Sequence ; Cognition Disorders ; genetics ; Molecular Sequence Data ; Mutation ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Risk Factors ; Sequence Analysis, DNA