Investigation of the effect for bisphenol A on oxidative stress in human hepatocytes and its interaction with catalase.

Bisphenol A (BPA) as a chemical raw material, is widely used in the manufacturing process of daily necessities. It was reported that BPA could induce oxidative stress, and catalase (CAT) can protect the body from oxidative stress. In this paper, the effect of BPA on CAT was carried out in vitro and in vivo. Firstly, we studied the effects of BPA on oxidative stress, cell viability and CAT activity in human hepatocytes, and the results of vitro experiments show that the survival rate of hepatocytes significant decreased along with the increase of BPA concentration. And when the BPA concentration was 100 µM, the hepatocyte survival decreased by 13.2%, ROS levels in the cells increased by 85%. However, the activity of intracellular CAT increased with the increasing concentration of BPA in 24 h. The results of vivo experiments showed that the activity of CAT in the high-dose group decreased by 29.1% compared with the control group. The long-term effects of BPA on rats reduced the CAT activity in liver, which reduced the resistance to oxidative stress. Meanwhile, the interaction mechanism between BPA and CAT at the molecule level was performed via multiple spectra methods and molecular docking, and the results illustrated that the structural change of CAT is mainly due to the strong combination of BPA with the residues of Trp185. In addition, the interaction mechanism between BPA and CAT were hydrophobic and electrostatic effect. This study provided experimental evidence for better understanding the toxicity of BPA.

[Effects of two controlled-release fertilizers with different proportions of N, P and K on the nutrient uptake and growth of Chrysanthemum morifolium Ramat].

A pot experiment was conducted to study the effects of two controlled-release fertilizers CRFA (4% resin-coated, N: P2O5: K2O = 14: 14: 14) and CRFB (4% resin-coated, N: P2O5: K2O = 20: 8:10) on the nutrient uptake and growth of Chrysanthemum morifolium, with common compound fertilizer CCF (N: P2O5: K2O = 15: 15: 15) as the control. Six treatments were installed, i. e., CCF1 (CCF, 6 g N x pot(-1)), CCF2 (CCF, 3 g N x pot(-1)), CRFA1 (CRFA, 6 g x pot(-1)), CRFA2 (CRFA, 3 g x pot(-1)), CRFB1 (CRFB, 6 g x pot(-1)), and CRFB (CRFB, 3 g x pot(-1)). On the 30th day of applying common compound fertilizer CCF1 and CCF2, soil available N, P and K contents were 163.29 and 145.26 mg x kg(-1), 180.39 and 163.13 mg x kg(-1), and 300.08 and 213.15 mg x kg(-1), respectively, and decreased rapidly since then. In treatments CRFA1, CRFB1, CRFA2, and CRFB, soil available N content increased slowly, and reached the peak on the 60th day after fertilizing, being 129.51, 138.65, 118.36, and 126.31 mg x kg(-1), respectively. Soil available P content had the same variation trend. Its maximum concentration was 169.54 and 133.46 mg x kg(-1) in treatments CRFA1 and CRFA2 on the 30th day after fertilizing, and 137.13 and 84.68 mg x kg(-1) in treatments CRFB1 and CRFB2 on the 60th day after fertilizing, and decreased slowly then. The agronomic traits such as leaf area, leaf area index, branch number, flowering rate, flower number, and flower diameter, etc., in treatments CRFA and CRFB were obviously better than those of the control, and CRFB was better than CRFA, suggesting that CRFB more matched the nutrient demand of C. morifolium. Under the conditions of present experiment, applying CRFB2 obtained the highest yield.

Protective effects of EUK4010 on beta-amyloid(1-42) induced degeneration of neuronal cells.

EUK4010 has been identified to exhibit an inhibitory effect on beta-amyloid (Abeta)(1-42)-induced loss of neuronal cell viability. Further studies demonstrated that EUK4010 attenuated the Abeta(1-42)-induced degeneration in both cultured rat hippocampal neurons and human neuroblastoma cells, as demonstrated by typical morphological changes, cell viability and the chip-based flow cytometric assay. Gene expression analysis using DNA microarray showed that the senescence marker calcium-binding protein, regucalcin (Rgn), GABA-A receptor pi subunit (Gabrp), the huntingtin binding protein, optineurin (Optn) and a semaphorin family plexin A3 similar protein (Plex-similar) changed their expression levels significantly in cultured neurons after Abeta(1-42) treatment. In this report, we have undertaken a chemical genetic approach to study the molecular basis of Abeta(1-42) effects on the neuronal degeneration. Our results demonstrate that EUK4010 completely blocked the Abeta(1-42)-induced up-regulation of GABA-A receptor pi subunit and the semaphorin family plexin A3 similar protein, and partially attenuated the down-regulation of senescence marker calcium-binding protein, regucalcin. These observations suggest that EUK4010 may prevent or reduce the Abeta toxicity by regulating the expression of genes involved in the Abeta induced neuronal degeneration. These genes may represent a promising target for the therapeutic drug development for Alzheimer's disease (AD) and other neurological disorders. Furthermore, EUK4010 and its analogues could potentially be developed as neuronal protective agents for the treatment of these diseases.