Convenient Colorimetric Detection of Thrombin via Aptamer-Mediated Inhibition and Restoration of the Oxidase Activity of Nanoceria.

Cerium oxide nanoparticles, also called nanoceria, have recently gained much attention as oxidase-mimicking nanozymes that catalyze the oxidation of chromogenic substrates for color generation without the addition of H2O2. Herein, we have developed a unique colorimetric biosensor for thrombin in human blood plasma, which relies on thrombin-binding aptamer (TBA)-mediated inhibition of the oxidase activity of nanoceria and its restoration by very selective interactions of TBA with target thrombin. In this system, nanoceria were first incubated with TBA, resulting in quick reduction of the oxidase activity of nanoceria via the adsorption of single-stranded (ss)DNA-type TBA on nanoceria. By the addition of sample solutions containing target thrombin, TBA bound on the nanoceria would strongly interact with free thrombin and be detached from the nanoceria, thereby increasing the available surface area of the nanoceria and consequently enhancing the oxidase activity. Using this strategy, target thrombin was successfully detected at concentrations as low as 100 pM over a wide linear range from 0.1 to 10 nM. The diagnostic capability of this method has been demonstrated by detecting thrombin in human blood plasma, showing its great potential in the practical applications.

Effect of manganese exposure on the neuroendocrine system in welders.

To evaluate the effect of occupational exposure to manganese (Mn) on serum prolactin (PRL) and the interrelationship among other hypophyseal-pituitary hormones, a cross-sectional study was conducted on 251 welders and 100 age-matched, office workers. We analyzed serum PRL, dopamine (DA), thyroid stimulating hormone releasing hormone (TRH), follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (TST) and measured current airborne Mn concentration in the welders. Cumulative exposure index (CEI) of airborne Mn was calculated. CEI and the present Mn level of the welders were 1.4+/-1.1mg/m3 year (range: 0.0-4.9) and 0.4+/-3.84 mg/m3 (range: 0.0-3.8), respectively. TRH, FSH and LH were higher in welders (5.08 pg/ml, 7.40 and 4.91 mIU/ml, respectively) than in office workers (3.91 pg/ml, 6.15 and 4.00 mIU/ml, respectively) (p<0.05). DA was decreased and TRH was increased significantly with increasing CEI. DA increased up to CEI 2.0mg/m3 year or mean Mn level up to 0.2mg/m3, then decreased. PRL showed increasing tendency above the CEI and mean Mn level at which DA started to decrease. PRL was positively associated with DA in the office workers. However, such a normal feedback control of DA on PRL was not observed in the welders. Structural equation model (SEM) analysis showed that CEI was positively related to TRH and negatively related to DA. TRH increased PRL. PRL increased LH and perhaps FSH, and on the other hand, decreased TST. These results showed that Mn suppresses the inhibitory feedback control of DA on the hypophyseal-pituitary axis. In conclusion, we postulate that suppressed dopaminergic inhibitory function on the hypophyseal-pituitary axis might be the mechanism for the increased PRL exhibited in the welders.

Pulmonary Toxicity and Recovery from Inhalation of Manual Metal Arc Stainless Steel Welding Fumes in Rats.

The objectives of this study were to examine the lung injury and inflammation caused by manual metal arc stainless steel (MMA-SS) welding fume inhalation and to evaluate the recovery process. Sprague-Dawley rats were exposed to MMA-SS welding fumes for 2 h per day in a whole-body exposure chamber, with a total suspended particulate (TSP) concentration of 51.4 ± 2.8 mg/m3 (low dose) or 84.6 ± 2.9 mg/m3 (high dose) for 30 days. The animals were sacrificed after 30 days of exposure as well as after a 30-day recovery period. To assess the inflammatory or injury responses, cellular and biochemical parameters as well as cytokines were assayed in the bronchoalveolar lavage fluid (BALF). MMA-SS welding fume exposure led to a significant elevation in the number of alveolar macrophages (AM) and polymorphonuclear cells (PMN). Additionary, the values of ß-nacetyl glucosaminidase (ß-NAG) and lactate dehydrogenase (LDH) in the BALF were increased in the exposed group when compared to controls. After 30 days of recovery from exposure, a significant reduction in inflammatory parameters of BALF was observed between the exposed and recovered groups. Slight, but significant elevations were noted in the number of AM and PMN in the recovered groups, and AM that had been ingested fume particles still remain in the lungs. In conclusion, these results indicated that welding fumes induced inflammatory responses and cytotoxicity in the lungs of exposed rats. Fume particles were not fully cleared from lungs even after a 30-day recovery period.