Subject(s)
Echinococcosis/diagnosis , Echinococcus granulosus/isolation & purification , Lymph Nodes/parasitology , Thoracic Neoplasms/diagnosis , Adult , Animals , Clavicle , Diagnosis, Differential , Echinococcosis/parasitology , Female , Humans , Lymph Nodes/pathology , Lymphatic Metastasis/diagnosisABSTRACT
OBJECTIVE: In this study, we investigated the association of two vitamin D receptor (VDR) polymorphisms BsmI and TaqI with colon cancer in a Caucasian population. METHODS: The VDR gene polymorphisms BsmI and TaqI were detected by polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP)-genotyping assays by using endonucleases BsmI and TaqI, and an agarose gel electrophoresis technique in a series of 43 colon cancer patients and 42 healthy controls. RESULTS: Allele frequencies and genotype distributions were found to be similar in both cases and controls. When homozygous carriers and heterozygotes were combined for each allele, alleles B and T were found to be more common in the control group (p=0.039, χ(2)=4.276, odds ratio [OR]=0.312, 95% confidence interval [CI]=0.100-0.973 and p=0.039, χ(2)=4.258, OR=0.254, 95% CI=0.064-1.000, respectively). When genotypes were analyzed as pairs, the Bb/TT variant was higher in the control group at a statistically high significance (p=0.001, χ(2)=11.854, OR=0.122, 95% CI=0.032-0.460). CONCLUSION: The alleles B and T and the genotype combination Bb/TT were found to be higher in the control group, and thus BsmI and TaqI polymorphisms of the VDR gene may be possible risk factors for colorectal carcinogenesis.
Subject(s)
Colonic Neoplasms/genetics , Polymorphism, Genetic/genetics , Receptors, Calcitriol/genetics , White People/genetics , Case-Control Studies , Deoxyribonucleases, Type II Site-Specific , Female , Gene Frequency , Genetic Predisposition to Disease , Genotype , Humans , Male , Middle Aged , Polymorphism, Restriction Fragment Length , TurkeyABSTRACT
Ulcerative colitis is a multifactorial inflammatory disease of the colon and rectum with an unknown etiology. The present study was undertaken to investigate the effect of melatonin administration on oxidative damage and apoptosis in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Rats were divided into four groups as follows: Group 1 (n=8)-T-NBS colitis; Group 2 (n=8)--melatonin, 10 mg/kg/day ip, for 15 days in addition to TNBS; Group 3 (n=8)--melatonin alone, 10 mg/kg/day ip, for 15 days; and Group 4 (n=8)-isotonic saline solution, 1 ml/rat ip, for 15 days (sham control group). Colonic myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels, and glutathione (GSH) levels are indicators of oxidative damage, while caspase-3 activities reveal the degree of apoptosis of the colonic tissue. In all TNBS-treated rats, colonic MPO activity and MDA levels were found to be increased significantly compared to those in the sham group. Colonic MPO activity and MDA levels were significantly lower in the melatonin treatment group compared to TNBS-treated rats. GSH levels of colonic tissues were found to be significantly lower in TNBS-treated rats compared to the sham group. Treatment with melatonin significantly increased GSH levels compared to those in TNBS-treated rats. Caspas-3 activity of colonic tissues was found to be significantly higher in TNBS-treated rats compared to the sham group. Treatment with melatonin significantly decreased caspase-3 activity compared to that in TNBS-treated rats. These results imply a reduction in mucosal damage due to anti-inflammatory and anti-apoptotic effects of melatonin.
