[Effect of astaxanthin on oxidative stress of red blood cells and peroxidation damage of membrane].

OBJECTIVE: To explore the effect of astaxanthin (ASTA) on oxidative stress of intra- and extra- red blood cells during stored period and the protective function for cell membrane. METHODS: The blood of volunteers was collected to prepare suspended red blood cells without leukocytes. Then the red blood cells were randomly divided into group A, group B, group C and group D. The ASTA was added into MAP preservation solution of group B, group C and group D, the final concentration of ASTA was 5, 10 and 20 µmol/L respectively. Group A was used as control group, in which only the dissolved liquid DMSO of ASTA was added. The red blood cells were stored in refrigerator at 2 °C-6 °C. On day 7, 14, 28 and day 42 of storage, the content of reactive oxygen species (ROS) in red blood cells was detected by fluorescence microplate reader. The content of malondialdehyde (MDA) was detected with TBA method. The content of hydrogen peroxide (H2O2) outside cell was detected with spectrophotometric method. The mean corpuscular volume(MCV) was detected with blood cell analyzer. The content of free hemoglobin(FHb) was detected with chemical colorimetry. RESULTS: The ROS, MDA, FHb and H2O2 levels in B, C and D groups were lower than those in control group during the stored period. On day 7 and 14 of storage, among group B, group C, group D and group A, the MCV showed no difference in comparison with control group. On day 28 and 42 of storage, the MCV in B, C and D groups was lower than that in control group. CONCLUSION: The ASTA can reduce the oxidative stress level of stored red blood cells inside and outside, relieve the peroxidation damage of cell membrane.

Polymorphism in the promoter region of the NFKB1 gene increases the risk of sporadic colorectal cancer in Swedish but not in Chinese populations.

OBJECTIVE: An insertion/deletion polymorphism (-94ins/delATTG) in the promoter region of the NFKB1 gene correlates to an increased risk of ulcerative colitis, a known risk factor for colorectal cancer, but this polymorphism has not been studied in colorectal cancer patients. The purpose of this study was to investigate whether this polymorphism is related to colorectal cancer risk and clinicopathological variables. MATERIAL AND METHODS: Case samples were taken from four groups of Swedish patients: 193 unselected patients, 90 patients with > or =3 affected 1st-degree relatives, 85 patients with 2 affected 1st-degree relatives, and 109 sporadic cancer patients, and one group of 193 unselected Chinese patients. Controls included 439 Swedish and 458 Chinese healthy individuals. Genotypes were determined by polymerase chain reaction (PCR)-restriction fragment length polymorphism. RESULTS: The deletion increased the risk of colorectal cancer among Swedish unselected patients (OR =3.81, 95% CI: 2.17-6.69, p <0.0001 for heterozygote deletion, and OR=4.65, 95% CI: 2.43-8.89, p <0.0001 for homozygote deletion) and sporadic cancer patients (OR =7.73, 95% CI: 3.06-19.57, p <0.0001 for heterozygote deletion, and OR =6.58, 95% CI: 2.35-18.43, p <0.0001 for homozygote deletion) compared to homozygote insertion (wild-type), but not among the other Swedish or Chinese patients (p >0.05). Similar evidence was seen in age-adjusted analyses (p <0.0001). The polymorphism did not correlate to clinicopathological variables (p >0.05). CONCLUSIONS: Deletion of the polymorphism was associated with increased susceptibility to sporadic colorectal cancers in the Swedish population, but not in the Swedish patients with a family history of colorectal cancer or in Chinese patients.

Association of NFKBIA polymorphism with colorectal cancer risk and prognosis in Swedish and Chinese populations.

OBJECTIVE: The inhibitory proteins, IkappaBs, regulate the activity of nuclear factor kappa-beta (NF-kappaB), which is implicated in tumorigenesis by regulating expression of a variety of genes involved in cellular transformation, proliferation, invasion, angiogenesis and metastasis. Variants in the genes encoding IkappaBs may be involved in cancer development through the activation of NF-kappaB. The objective of this study was to investigate the susceptibility of an A to G variation (rs696) in the 3' UTR of NFKBIA (encoding IkappaBalpha) to colorectal cancer (CRC) and the association of this polymorphism with clinicopathologic variables in CRC patients. MATERIAL AND METHODS: A case-control study was carried out on a Swedish (155 CRCs, 438 controls) and a Chinese population (199 CRCs, 577 controls). The genotype of NFKBIA was determined by PCR-restriction fragment length polymorphism. RESULTS: The frequency of the AG genotype was increased in the Chinese patients >or=50 years of age compared with the Chinese controls (odds ratio (OR)=3.06, 95% confidence interval (CI)=1.55-6.02, p=0.001), even when adjusted for age (OR=3.20, 95% CI=1.61-6.38, p=0.001). The GG genotype of NFKBIA was related to a poorer survival rate in the Swedish patients, independent of gender, age, tumour location, Dukes' stage and differentiation (hazard ratio = 3.10, 95% Cl=1.28-7.60, p=0.01). CONCLUSIONS: Chinese individuals >or=50 years of age carrying the AG genotype of NFKBIA may be at an increased risk of developing CRC, and the GG genotype of NFKBIA may be considered as a prognostic factor for Swedish CRC patients.

Genetic polymorphisms of N-acetyltransferase 2 and colorectal cancer risk.

AIM: To identify the distribution of N-acetyltrasferase 2(NAT2) polymorphism in Hebei Han Chinese and the effects of the polymorphism on the development of colorectal cancer. METHODS: We performed a hospital-based case-control study of 237 healthy individuals and 83 colorectal cancer patients of Hebei Han Chinese. DNA was extracted from peripheral blood and cancer tissues. The genotypes of the polymorphisms were assessed by PCR-restriction fragment length polymorphism (RFLP). RESULTS: There were four NAT2 alleles of WT, M1, M2, and M3 both in the healthy subjects and in the patients, and 10 genotypes of WT/WT, WT/M1, WT/M2, WT/M3, M1/M1, M1/M2, M1/M3, M2/M2, M2/M3, M3/M3. M2 allele was present in 15.61% of healthy subjects and 29.52% of patients (chi(2) = 15.31, P<0.0001), and M3 allele was present in 30.59% of healthy subjects and 16.87% of patients (chi(2) = 25.33, P<0.0001). There were more WT/M2 (chi(2) = 34.42, P<0.0001, odd ratio = 4.99, 95%CI = 2.27-9.38) and less WT/M3 (chi(2) = 3.80, P = 0.03) in the patients than in the healthy subjects. In 70.3% of the patients, there was a difference in NAT2 genotype between their tumors and blood cells. Patients had more WT/M2 (chi(2) = 5.11, P = 0.02) and less M2/M3 (chi(2) = 4.27, P = 0.039) in their blood cells than in the tumors. Furthermore, 53.8% (7/13) of M2/M3 in tumors were from WT/M2 of blood cells. CONCLUSION: There is a possible relationship between the NAT2 polymorphisms and colorectal cancer in Hebei Han Chinese. The genotype WT/M2 may be a risk factor for colorectal cancer.