Heavy Metal Components in Blood and Urinary Stones of Urolithiasis Patients.

Lifestyle, food intake, and exposure to chemicals are potential risk factors for the development of calcium urolithiasis. Pb, Cd, and Hg have been proved to cause renal illness, and urinary tract stones might be caused by exposure to metals. Therefore, this study aimed to measure the concentration of metals in urinary tract stones and blood simultaneously in urolithiasis patients. Moreover, we intended to determine whether urinary tract stones can be regarded as a biomarker of exposure or an effect marker in a population with environmental exposure to metals. Thirty-five urolithiasis patients (case) and 34 healthy inhabitants (control) were recruited in this study. The contents of Pb, Cd, Cr, Cu, Ni, As, Zn, and Hg were determined in urinary stones and blood in the case and control groups. The most abundant metals were Zn and Cu in blood and Zn and Ni in urinary stones. Significantly higher levels of Zn, Ni, and As were found in calcium phosphate stones than in calcium oxalate or uric acid stones. The majority of metals were not present at consistent levels in both blood and urinary stones, except for Zn. Urinary stones might be explained as providing another metabolic pathway for metal contamination. Moreover, as the metals with the highest content in urinary stones were Ni and Zn, and Ni content was very much higher than in other countries, contamination by Ni should be further taken into consideration if there is any serious contamination in Taiwan.

Oxidative damage in patients with benign prostatic hyperplasia and prostate cancer co-exposed to phthalates and to trace elements.

Evidence indicates that prostates exposed to environmental endocrine disruptors and trace metals will cause adverse health outcomes. We assessed the association between urinary phthalate metabolites and serum trace metal levels, and oxidative damage in benign prostatic hyperplasia (BPH) patients, prostate cancer (PCa) patients, and healthy controls. Levels of cadmium (Cd), nickel (Ni), and copper (Cu) were significantly higher in BPH patients than in controls, and mercury (Hg) was highest in PCa patients. An Hg level >1 µg/L posed a significant risk (OR: 42.86, 95% CI: 1.092-1684) for PCa, but a zinc (Zn) level >1 µg/L was marginally negative (OR: 0.979, 95% CI: 0.957-1.002). We also found strong associations between PCa and mono-isononyl phthalate (MiNP), and between BPH and mono-isodecyl phthalate (MiDP), malonyldialdehyde (MDA) were significantly higher in PCa and BPH patients than in controls; 8­hydroxydeoxyguanosine (8­OH­dG) and DNA strand breakage were highest in BPH patients and lowest in controls. When the prostate was simultaneously co-exposed to phthalates and trace metals, phthalates had a less significant effect on PCa and BPH. Thus, we hypothesize that, for patients with prostate disease, exposure to trace metals is more significant than is exposure to phthalates.

In-chern-hau-tang and genipin reduces acute urinary bladder distension evoked sympathetic activation-induced hepatic dysfunction in rats.

Increased norepinephrine production by acute urine retention (AUR) induced sympathetic activation may contribute to acute liver injury (ALI) via the action of hepatic vasoconstriction and increased reactive oxygen species (ROS) production. We evaluated whether In-Chern-Hau-Tang, a hepatoprotective herb medicine, and its major ingredient genipin, may ameliorate norepinephrine-induced liver injury in the rat. We determined the effects of In-Chern-Hau-Tang and genipin on norepinephrine-induced oxidative stress in the Kupffer and endothelial cells and AUR-induced ALI in the rat via a chemiluminescence analyzer, physiologic and biochemical determination and western blot. The results of in vitro study showed that genipin with efficient H(2)O(2) and HOCl scavenging activities decreased norepinephrine-enhanced ROS production in the Kupffer cell and endothelial cell cultures. AUR activated hepatic sympathetic nervous activity lead to a hepatic hypoxia/hypoperfusion, and a reduction in bile flow. AUR increased intercellular adhesion molecular 1 (ICAM-1) protein expression, and hepatic ROS production from the activated leukocyte NADPH oxidase activity subsequently leading to plasma aspartate aminotransferase (AST) elevation. Hepatic sympathetic denervation, or oral pretreatment of In-Chern-Hau-Tang or genipin for 1 week ameliorated the level in AUR-induced hepatic hypoxia/hypoperfusion, and bile stasis. Hepatic denervation, In-Chern-Hau-Yang and genipin inhibited AUR-enhanced hepatic ICAM-1 expression, hepatic ROS production, leukocyte NADPH oxidase activity and plasma AST activity. In conclusion, In-Chern-Hau-Tang along with its active component, genipin, can ameliorate AUR-induced ALI via the alleviation of oxidative stress possibly by the inhibition of sympathetic induced hypoxia/hypoperfusion and leukocyte NADPH oxidase activity.