Status and Interrelationship of Zinc, Copper, Iron, Calcium and Selenium in Prostate Cancer.

Deficiency or excess of certain trace elements has been considered as risk factor for prostate cancer. This study was aimed to detect differential changes and mutual correlations of selected trace elements in prostate cancer tissue versus benign prostatic hyperplasia tissue. Zinc, copper, iron, calcium and selenium were analysed in histologically proven 15 prostate cancer tissues and 15 benign prostatic hyperplasia tissues using atomic absorption spectrophotometer. Unpaired two tailed t test/Mann-Whitney U test and Pearson correlation coefficient were used to compare the level of trace elements, elemental ratios and their interrelations. As compared to benign prostatic tissue, malignant prostatic tissue had significantly lower selenium (p = 0.038) and zinc (p = 0.043) concentrations, a lower zinc/iron ratio (p = 0.04) and positive correlation of selenium with zinc (r = 0.71, p = 0.02) and iron (r = 0.76, p = 0.009). Considerably divergent interrelationship of elements and elemental ratios in prostate cancer versus benign prostatic hyperplasia was noted. Understanding of differential elemental changes and their interdependence may be useful in defining the complex metabolic alterations in prostate carcinogenesis with potential for development of element based newer diagnostic, preventive and therapeutic strategies. Further studies may be needed to elucidate this complex relationship between trace elements and prostate carcinogenesis.

SRD5A2 gene polymorphisms and the risk of benign prostatic hyperplasia but not prostate cancer.

BACKGROUND: Testosterone, a primary androgen in males, is converted into its most active form, dihydrotestosterone (DHT), by 5α-reductase type 2 (encoded by the SRD5A2 gene) in the prostate. DHT is necessary for prostatic growth and has five times higher binding affinity than testosterone for androgen receptors. We hypothesized that polymorphic variations in the SRD5A2 gene may affect the risk of benign prostatic hyperplasia and prostate cancer. MATERIALS AND METHODS: We analyzed SRD5A2 gene polymorphisms in 217 BPH patients, 192 PCa cases, and 171 controls. Genotyping was undertaken using direct DNA sequencing. Genotype data were compared between cases and controls using a Chi square statistical tool. RESULTS: We found that the A49T locus was monomorphic with 'AA' genotype in all subjects. At V89L locus, the presence of 'VV' showed a marginally significant correlation with increased BPH risk (p=0.047). At the (TA)n locus, longer TA repeats were found to be protective against BPH (p=0.003). However, neither of these polymoprhisms correlated with the risk of PCa. CONCLUSIONS: We conclude that A49T is monomorphic in the study population, VV marginally correlates with BPH risk, and longer (TA)n repeats are protective against BPH. None of these polymorphisms affect the risk of PCa.

Null genotypes at the GSTM1 and GSTT1 genes and the risk of benign prostatic hyperplasia: a case-control study and a meta-analysis.

BACKGROUND: Benign prostatic hyperplasia (BPH) is an age related non-malignant disease diagnosed as lower urinary tract symptoms and prostatic enlargement. Null genotypes in drug detoxification glutathione-S-transferase genes/enzymes, such as GSTT1 and GSTM1 have been reported to increase risk of several cancers including prostate. Meta-analysis on PC also suggested significant impact of GSTM1 null genotype but not that of GSTT1; however, BPH data have not been subjected to meta-analysis. METHODS: We investigated GSTT1 and GSTM1 genotypes in 429 subjects which included 244 BPH, 51 prostate cancer (PC) patients, and 134 control subjects to find if null genotype in any of the two genes increased the risk of BPH/PC. We also performed a quantitative meta-analysis on 888 BPH cases and 793 controls for GSTM1 and on 890 BPH cases and 793 controls for GSTT1 to assess overall consensus about the impact of null genotypes on BPH risk. RESULTS: We did not find any significant difference in the distribution of genotypes of either of the two genes between BPH/PC cases and controls; however, double deletion (GSTM1 null + GSTT1 null) increased BPH risk, significantly. Upon meta-analysis, null genotype of GSTM1 but not that of GSTT1 appeared to strongly affect BPH risk. CONCLUSIONS: In our population, null genotypes of either GSTM1 or GSTT1 do not appear to affect BPH risk; however, the double deletion was significantly associated with BPH. Meta-analysis suggested significant influence of GSTM1 null genotype but not that of GSTT1 on BPH risk.