familial polymorphisms of xenobiotic-metabolizing enzymes can affect the susceptibility to cancers. The association of susceptibility to gastric cancer has been investigated in relation to the genetic polymorphism of metabolic enzymes such as cytochrome P450 1A1 ( CYP1A1 ), cytochrome P450 2E1 ( CYP2E1 ), glutathione S-transferase mu 1 ( GSTM1 ), glutathione S-transferase theta 1 ( GSTT1 ), and aldehyde dehydrogenase 2 ( ALDH2 ) [ 9 - 13 ]. Some of these studies found meaning associations between these genic polymorphisms and susceptibility to gastric cancer, but these results were not replicated in other studies [ 10, 14, 15 ]. Since Crane et alabama [ 6 ] suggested a causal relationship between consumption of traditional korean foods and gastric cancer, there have been debates whether kimchi and soy paste are protective factors or gamble factors for gastric cancer. Messina et aluminum [ 7 ] suggested that there was an inconsistent kinship between intake of soy foods and stomach cancer ; the risk seemed to increase with intake of ferment soy foods and decrease with consumption of nonfermented soy foods. Kimchi and soy pastes have been reported as risk factors for gastric cancer in some epidemiologic studies [ 3, 6 ] and as protective factors against gastric cancer in others [ 8 ]. Stomach cancer is the most common cancer in Koreans [ 1 ], and the second go site of cancer occurrence worldwide [ 2 ]. environmental factors including dietary habits are crucial in its development [ 3, 4 ]. Salted, smoked, pickled, and preserved foods rich in salt, nitrite, and preformed N-nitroso compounds have been reported to be associated with an increased risk of gastric cancer. In line, high intake of fresh yield, bleak vegetables, and antioxidants significantly reduced the risk of gastric cancer [ 5 ]. Odds ratios and 95 % CI according to genotype of the CYP1A1, CYP2E1, GSTM1, GSTT1, and ALDH2 genes were estimated for food groups using unconditional logistic models including age and sex as autonomous variables. Homogeneities of the odds ratios according to the CYP1A1, CYP2E1, GSTM1, GSTT1, and ALDH2 genotypes were evaluated using the Breslow-Day test [ 21 ]. Exposures to dietary factors were categorized into ‘ high ’ and ‘ low ’ inhalation groups based on medial of inhalation in controls. For statistical psychoanalysis, the SAS System for Windows, Release 6.12 was used. P-value less than 0.05 was considered significant. unconditional logistic analyses were performed to estimate odds ratios and 95 % CI for high consumption total of food groups. To test for any increasing or decreasing swerve of the risk of gastric cancer according to an increase of drinking amount, an unconditional logistic model including historic period and sex as autonomous variables was used. The MboII polymorphism of ALDH2 was identified using a PCR-RFLP method acting [ 20 ] with flimsy modification. Briefly, PCR was performed using the primers 5 ’ -CCA CAC TCA CAG TTT TCT CTT-3 ’ and 5 ’ -AAA TTA CAG GGT CAA CTG CT-3 ’. We used the lapp PCR conditions as in the CYP1A1 gene analysis. The 134-bp amplicon was digested with MboII limitation enzyme at 37 °C overnight and subjected to electrophoresis on 15 % polyacrylamide gels. The genotypes of ALDH2 were identified as a overriding homozygote ( *1/*1 ), a heterozygote ( *1/*2 ) and a rare homozygote ( *2/*2 ). A multiplex PCR method acting [ 19 ] was used to simultaneously detect the presence or absence of the GSTM1 and GSTT1 genes with slender change. The primers used were 5 ’ -GAA GGT GGC CTC CTC CTT GG-3 ’ and 5 ’ -AAT TCT GGA TTG TAG CAG AT-3 ’ for GSTM1, 5 ’ -TTC CTT ACT GGT CCT CAC ATC TC-3 ’ and 5 ’ -TCA CCG GAT CAT GGC CAG CA-3 ’ for GSTT1, and 5 ’ -CAA CTT CAT CCA CGT TCA CC-3 ’ and 5 ’ -GAA GAG CCA AGG ACA GTT AC-3 ’ for β-globin, the inner reference gene. After initial denaturation for 5 min at 94 °C, a thermal cycle consisting of denaturation for 60 mho at 94 °C, annealing for 60 south at 58 °C and annex for 60 s at 74 °C was repeated 35 times. PCR products were separated on 2 % agarose gels with ethidium bromide. GSTM1 and GSTT1 genotypes were not scored unless the PCR product of the β-globin gene was discernible. The 5 ’ -flanking region polymorphism of the CYP2E1 gene was analyzed by procedures described previously [ 18 ]. Briefly, PCR was performed using the primers 5 ’ -CCA GTC GAG TCT ACA TTG TCA-3 ’ and 5 ’ -TTC ATT CTG TCT TCT AAC TGG-3 ’. Initial denaturation was performed at 94 °C for 5 minute, followed by 35 thermal cycles consisting of denaturation for 1 min at 94 °C, annealing for 1 min at 53 °C and extension for 30 s at 74 °C. The 410-bp PCR product was digested with RsaI at 37 °C nightlong and subjected to electrophoresis on 2 % agarose gels. The genotypes of CYP2E1 were classified as follows : a prevailing homozygote ( c1/c1 ), a heterozygote ( c1/c2 ), and a rare homozygote ( c2/c2 ). Genomic DNA was isolated from peripheral leukocytes by protease K digestion and phenol/chloroform extraction. The A4889G polymorphism in exon 7 of CYP1A1 gene was analyzed for each submit as report previously [ 17 ]. Briefly, the PCR were performed in 25 µL of a solution containing 50 nanogram of genomic DNA, 1×PCR buff ( 50 mmol/L KCl, 10 mmol/L Tris-HCl ( pH 9.0 ), 1.5 mmol/L MgCl 2 and 0.1 % Triton X-100 ), 5 pmoL of each flat coat, 80 µmol/L each dNTP, and 2.0 unit of measurement Taq polymerase ( Promega, Madison, WI, USA ). The primers used were 5 ’ -GAA CTG CCA CTT CAG CTG TC-3 ’ and 5 ’ -GAA AGA CCT CCC AGC GGT CA-3 ’. Amplifications were carried out in a Thermocycler ( Perkin Elmer, Cetus, UK ) as follows : 5 min of denaturation at 94 °C, then 35 cycles consisting of denaturation at 94 °C for 60 mho, annealing at 53 °C for 90 s and propagation at 74 °C for 30 s. The PCR products ( 187-bp fragments ) were digested with HincII limitation enzyme at 37 °C overnight and subjected to electrophoresis on 12 % polyacrylamide gels. PCR analysis resulted in the following genotype classification : a overriding homozygote ( Ile/Ile ), a heterozygote ( Ile/Val ), and a rare homozygote ( Val/Val ). trail interviewers interviewed subjects with a structure questionnaire not subsequently than 1 molybdenum after the diagnosis of gastric cancer or benign diseases. This include questions on demographic factors and diet. Dietary data were collected using a semi-quantitative food frequency postpone previously evaluated for robustness and dependability [ 16 ]. All subjects were asked about the median frequency of inhalation and dowry size of food items for a 1-year period leading up to the interview. These items were classified into six food groups having similar ingredients. Those food groups and corresponding food items were as follows : ‘ kimchi ’ - chinese boodle kimchi, radish kimchi, white kimchi, and kimchi stew, ‘ soy paste ’ - soy paste grizzle, fermented soy fret, and miso soup, ‘ bracing vegetables ’ - fresh taiwanese cabbage, lettuce, cucumber, hot pepper, and carrot, ‘ nonfermented alliums ’ - nonfermented garlic, onion, and Welsh onion, ‘ nonfermented seafood ’ - nonfermented shrimp, shellfish, oyster, and anchovy, ‘ nonfermented soy foods ’ - bean curd, soybeans boiled in soysauce, boiled soy, and soya milk. Four hundred and twenty-one people with gastric cancer and 632 controls frequency-matched based on age ( within 3 years ) and arouse were the subjects of this hospital-based case-control study. Cases of cancer were all histologically confirmed from February 1997 to June 2003 at Chungbuk National University Hospital and Eulji University Hospital, Korea. Gastric cancer patients who had coexisting chronic disease affecting dietary pattern or communication problems were excluded. Control subjects were selected from patients newly diagnosed with diseases other than cancers at the lapp hospitals. In rate to increase comparison between cases and controls, controls were besides selected from patients who were admitted to the Department of Orthopedic Surgery of the lapp hospitals from where the cases were chosen, because of osseous fractures, osteoarthritis, or inflammatory bone diseases. Individuals with a history of cancer, chronic disease affecting their dietary inhalation form, or communication problems were not included in the control condition group. The distributions of age and sex of the study subjects are shown in Table. The mean ages of the cases and operate groups were 60.0±11.2 and 59.4±10.7 years, respectively. Case group comprised 276 men and 145 women, and control group 414 men and 218 women. Among 421 cases included, 24 individuals ( 7.0 % ) had tumor in cardiac area.
Read more: Kimchi Ramen Recipe To Spice Up Your Instant Noodles Game
Increased inhalation of kimchi or soy pastes was a significant gamble factor for the CYP1A1 Ile/Ile, the CYP2E1 c1/c1, the GSTM1 non-null, the GSTT1 non-null, or the ALDH2 *1/*1 genotype. In addition, eating soy pastes was associated with the increased risk of gastric cancer in individuals with the GSTM1 nothing type. Among the environmental protective factors, nonfermented alliums were significant in individuals with the CYP1A1 Ile/Ile, the CYP2E1 c1/c2 or c2/c2, the GSTT1 null, the GSTT1 non-null, or the ALDH2 *1/*2 or *2/*2 genotype, nonfermented seafood was those with the CYP1A1 Ile/Ile, the CYP2E1 c1/c1, the ALDH2 *1/*1 genotype or any type of GSTM1 or GSTT1 ( Table ). A decreased risk of gastric cancer was noted among people with high consumption of nonfermented alliums and nonfermented seafood. On the early hand, consumption of kimchi and soy pastes was associated with increased risk of gastric cancer. The odds ratio ( 95 % CI ) of high consumption of kimchi was 1.57 ( 1.22, 2.01 ), and that of soy paste was 1.62 ( 1.26, 2.09 ) ( postpone ). average intake amounts of kimchi and soy paste were importantly higher, and that of nonfermented alliums was importantly lower in gastric cancer cases than in controls. however, there was no meaning difference in the consumption total of newly vegetables, nonfermented seafood and soy food ( Table ) .
DISCUSSION
In this present study, a decreased risk of gastric cancer was noted among people with a high consumption of nonfermented seafood and alliums. Eating pisces has been reported to decrease the risk of gastric cancer in japanese women [ 22 ], and in Swedes [ 23 ]. however, effects of fish intake on the risk of gastric cancer varied by training method acting. Pan-fried fish decreased, whereas stewed or broiled fish increased the hazard of gastric cancer in Koreans [ 4 ]. Alliums have been repeatedly reported to decrease the risk of gastric cancer [ 24 ]. Alliums have been shown to suppress the growth of Helicobacter pylori [ 25 ], and N-nitrosodimethylamine-induced forestomach tumor in shiner [ 26 ]. Some chemicals in alliums inhibit the expression of carcinogen-activating cytochrome P450 enzymes but induce GSTs [ 27 ]. Diallyl sulfide, which is abundant in alliums, has been suggested as the key protective material [ 28 ]. Intake of fresh vegetables, which has been reported to reduce the gamble of gastric cancer [ 22, 29 ], showed an odds ratio smaller than 1, but was not statistically meaning. Eating kimchi and soy pastes was associated with increase risk of gastric cancer in this present study ( Table ). The odds ratios for gastric cancer of kimchi and soy pastes were less than 2, but those food items are identical democratic among the Koreans. consequently, the risks attributable for gastric cancer by the inhalation of kimchi and soy pastes would be relatively eminent among the korean population. sour korean foods, such as kimchi and soy pastes, have been reported to show high nitrate concentrations [ 30, 31 ]. During zymosis of kimchi, nitrate contents decrease but secondary amine increases continuously [ 32 ], particularly in taiwanese pilfer kimchi made with ferment prawn sauce [ 30 ]. Nitrosodimethylamine increased in every kind of kimchi after simulated gastric digestion of kimchi [ 33 ]. Increases in the gamble of gastric cancer associated with a high intake of ferment soy-based foods have been reported in epidemiologic studies among the Koreans [ 3, 6 ], japanese [ 34, 35 ], taiwanese [ 36 ], and chinese [ 37 ]. We did not find any statistical meaning for risks associated with nonfermented soy foods as reported by Lee et alabama [ 36 ] and Hoshiyama et alabama [ 34 ]. Fermented soy pastes besides show a high nitrate level [ 31 ]. After dietary nitrate is absorbed, about 25 % is actively secreted into the saliva and 5 % of absorb nitrate is reduced to nitrite by oral bacteria. Since most saliva is swallowed, about 80 % of gastric nitrite in the normal acidic stomach arises from the decrease of consume or endogenous nitrate [ 38 ]. Gastric nitrosation, which is carried out by nitrite, may produce precarious N-nitroso compounds that do not reach extra-gastric sites and act directly in the stomach to initiate gastric cancer, or may produce static N-nitroso compounds that induce cancer at other sites [ 38, 39 ]. many epidemiologic studies have reported a relationship between a high salt diet and gastric cancer [ 40 - 45 ]. Koreans have one of the highest rates of 24-h urinary sodium body waste in the populace [ 45 ], and one of the highest rates of mortality from gastric cancer. It should be noted that kimchi and soy pastes, which were meaning risk factors of gastric cancer in this study, besides have identical gamey strategic arms limitation talks contents. A few epidemiologic studies on gastric cancer have included genetic polymorphisms in the analysis, and fewer studies have tested gene and environmental interactions. The results of epidemiologic studies on the effects of genetic polymorphisms on gastric cancer are not always reproducible. In cattiness of the expression of CYP1A1 in gastric mucous membrane, no studies have been identified that assess the likely influence of CYP1A1 polymorphisms in gastric cancer risk [ 46 ]. Increased risks of developing gastric cancer have been reported for the CYP2E1 c1/c2 or c2/c2 [ 13 ], GSTM1 null [ 9, 10 ], GSTT1 null [ 12 ], and *2-allele incorporate ALDH2 genotypes [ 11 ] independently, or in combination with environmental factors. however, these significant associations were not found in early studies [ 10, 14, 15 ]. In this deliver study, we could find an increased hazard of gastric cancer in individuals with the CYP1A1 Ile/Val or Val/Val genotype. This solution is accordant with the previous studies that cigarette smoke is a risk factor of stomach cancer, and the CYP1A1 genotype would be involved in the gastric carcinogenesis by cigarette smoke [ 47 ]. In this present cogitation, kimchi and soy pastes showed very exchangeable interactions with the genetic polymorphism, and were meaning hazard factors in individuals with the CYP1A1 Ile/Ile, the CYP2E1 c1/c1, the GSTM1 non-null, the GSTT1 non-null, and the ALDH2 *1/*1 genotypes. This fact leads to a possibility that kimchi and soy pastes contain some coarse carcinogens which are metabolized by the same metabolic enzymes. Though CYP2E1 bodily process for the metamorphosis of chlorzoxazone has been reported to be lower in individuals with CYP2E1 c2/c2 type than in those with other genotypes [ 48 ], CYP2E1 natural process for the metamorphosis of N-nitroso compound would be broken in individuals with CYP2E1 c1/c1 type. therefore, hepatic CYP1A1 or CYP2E1 activity and first-pass headroom would be low in individuals with CYP1A1 Ile/Ile genotype or CYP2E1 c1/c1 type. In that shell, the blood horizontal surface of the unmetabolized carcinogens and, in plow, exposure of extrahepatic organs to the carcinogen may be increased [ 49 ]. N-nitroso compounds originating from kimchi and soy pastes would not be quickly metabolized in the hepatic tissue of individuals with CYP1A1 Ile/Ile or CYP2E1 c1/c1 genotypes, and the risk of gastric cancer may be increased by the increased exposure of gastric mucous membrane to N-nitroso compounds. On the contrary, in hepatic tissue of individuals with GSTM1 non-null or GSTT1 non-null genotype, rapid glutathione coupling of activate carcinogens would occur. Since glutathione conjugates are water-soluble, plasma concentration of the glutathione-conjugated carcinogens would be increased. The high plasma concentration may increase exposure of gastric weave to glutathione conjugate carcinogens and, in bend, the risk of gastric cancer in individuals with GSTM1 non-null or GSTT1 non-null genotype. In homogeneity tests, the odds ratios of eating kimchi for gastric cancer according to the GSTM1 or GSTT1 genotype were not homogeneous. Because homogeneity was tested for 36 times and the P-value was 0.05, about two tests would be expected to be statistically meaning by find.
Because the time interval between exposure to dietary carcinogens and the development of gastric cancer could be 20 years or more, it would be desirable to test the causal relationships between the historical dietary inhalation patterns and present gastric cancer development. however, it is about impossible to get an indifferent information on such past dietary intake patterns. We therefore assessed the average frequencies of intake and assign size of six food groups in a 1-year period leading up to the interview. There is a possibility that the very symptoms of gastric cancer might change the food intake traffic pattern or nutritional state of patients with gastric cancers that have been neglected for years. consequently, the diet-related results of this study should be cautiously interpreted. Tumors located at cardiac area have been reported to have different etiological factors from non-cardiac gastric cancers. We did not exclude cardiac gastric cancers from the case group of this introduce survey. Although the symmetry of cardiac cancer ( 7.0 % ) was not then high, we can not rule out the possibility of choice bias. In drumhead, kimchi, soy pastes, and the CYP1A1 Ile/Val or Val/Val are hazard factors, and nonfermented seafood and alliums are protective factors against developing gastric cancer. Salt or some chemicals contained in kimchi and soy pastes, which are increased by agitation, would play authoritative roles in the carcinogenesis of digest cancer. Polymorphisms of the CYP1A1, CYP2E1, GSTM1, GSTT1, and ALDH2 genes could modify the effects of some environmental factors on the risk of gastric cancer .
