Remediation of AMD Contaminated Soil by Two Types of Reeds

Acid mine drainage (AMD) adversely impacts many regions in the world. The interactions among citric acid (CA), rhizosphere bacteria and metal uptake in different types of Phragmites australis cultured in spiked AMD contaminated soil were investigated. Compared with non-contaminated reeds cultured under the same conditions, wild reeds harvested from a contaminated site accumulated more metals into tissues. Rhizosphere iron oxidizing bacteria (Fe(II)OB) enhanced the development of Fe plaque but had no significant impact on the formation of Mn and Al plaque on the root surface of either reeds. Plaque may restrain the accumulation of Fe and Mn into tissues of reeds. CA inhibited the growth of Fe(II)OB, reduced the formation of metal plaque and significantly elevated metal accumulations into both underground and aboveground biomass of reeds. The concentrations of Fe, Al and Mn were higher in belowground organs than aboveground tissues. The roots contained 0.28 ± 0.01 mg/g Mn, 3.09 ± 0.51 mg/g Al, 94.47 ± 5.75 mg/g Fe, while the stems accumulated 0.19 ± 0.01 mg/g Mn, 1.34 ± 0.02 mg/g Al, 10.32 ± 0.60 mg/g Fe in wild reeds cultured in soil added with 33,616 ppm CA. Further field investigations may be required to study the effect of CA to enhance phytoremediation of metals from real AMD contaminated sites.     

Plant-derived phenolic compounds impair the remediation of acid mine drainage using treatment wetlands

The use of wetlands to remediate acid mine drainage has expanded rapidly since the realisation that acid coal mine drainage running into natural sphagnum wetlands undergoes an increase in pH and a precipitation of metals. However, our study suggests that the inclusion of plants in the acid mine drainage treatment system may be questionable, due to inefficiencies caused by exudation of dissolved organic carbon (DOC), and in particular its phenolic constituents. They complex with iron, causing increased solubility, the exact opposite of what is required to facilitate amelioration. The addition of minewater to planted wetland mesocosms initially caused a decline in Fe concentrations, typically from over 1100 to a low of 75 mg L⁻¹. However, it increased higher than 300 mg L⁻¹ after 15 days. The rise in iron occurred concurrently with DOC and phenolic increases; 15-69 and 5-15 mg L⁻¹, respectively, for Eriophorum angustifolium. Removal of DOC by precipitation with calcium lowered the DOC abundance, but without a simultaneous decrease in iron concentration. The concentration of one fraction of the DOC, phenolic compounds, did not decline, and we propose that the Fe was complexed with that phenolic DOC pool. The proposal was confirmed by enzymic depletion of the phenolic compounds using phenol oxidase. Our findings suggest that phenolic complexation represents a potent constraint on wetland-based bioremediation of iron in acid mine drainage.     

Alpha-melanocyte stimulating hormone protects retinal pigment epithelium cells from oxidative stress through activation of melanocortin 1 receptor–Akt–mTOR signaling

Patients with age related macular degeneration (AMD) will develop vision loss in the center of the visual field. Reactive oxygen species (ROS)-mediated retinal pigment epithelium (RPE) cell apoptosis is an important contributor of AMD. In this study, we explored the pro-survival effect of α-melanocyte stimulating hormone (α-MSH) on oxidative stressed RPE cells. We found that α-MSH receptor melanocortin 1 receptor (MC1R) was functionally expressed in primary and transformed RPE cells. RPE cells were response to α-MSH stimulation. α-MSH activated Akt/mammalian target of rapamycin (mTOR) and Erk1/2 signalings in RPE cells, which were inhibited by MC1R siRNA knockdown. α-MSH protected RPE cells from hydrogen peroxide (H₂O₂)-induced apoptosis, an effect that was almost abolished when MC1R was depleted by siRNA. α-MSH-mediated S6K1 activation and pro-survival effect against H₂O₂ was inhibited by Akt inhibitors (perifosine, MK-2206 and LY294002). Further, mTOR inhibition by rapamycin, or by mTOR siRNA knockdown, diminished α-MSH’s pro-survival effect in RPE cells. Thus, Akt and its downstream mTOR signaling mediates α-MSH-induced survival in RPE cells. In summary, we have identified a new α-MSH–MC1R physiologic pathway that reduces H₂O₂-induced RPE cell damage, and might minimize the risk of developing AMD.     

Microperimetric Biofeedback in AMD Patients

To analyse biofeedback training by microperimeter MP-1 (Nidek Technologies) on patients with Age Related Maculopathy (AMD). We enrolled 15 patients (10 female and 5 male) and examined total of 27 eyes with AMD. All the patient underwent 10 training sessions of 10 min for each eye, performed once a week using the MP-1 biofeedback examination. Statistical analysis was performed using Student’s t-test. p values less than 0.05 were considered statistically significant. All patients displayed an improvement in visual acuity, fixation behaviour, retinal sensitivity an reading speed. The mean character size value improved from 36.4 to 11.7; this result was statistically significant (p = 0.031). A biofeedback examination using the MP-1 microperimeter can help the brain to memorize the final fixation location by increasing attention modulation, thereby providing an efficient preferred retinal locus for visual tasks in patients with macular disease and central scotoma.     

Expression of adiponectin in choroidal tissue and inhibition of laser induced choroidal neovascularization by adiponectin

The aim of this study was to investigate the role of adiponectin (APN) in a mouse model of laser induced choroidal neovascularization (CNV). We have shown by immunohistochemistry that the expression of APN, adiponectin receptor 1, adiponectin receptor 2 and T cadherin gradually increased from day 1 to day 7 post-laser in laser treated mice compared to controls. Recombinant APN (rAPN) was injected intraperitoneally (i.p., 25 microg/mouse) or intravitreally (2 microg/eye) in lasered mice. Another set of lasered mice received APN peptide via i.p. (75 microg/mouse) or intravitreal (30 microg/eye) route. Control mice received a similar treatment with PBS, control protein or control peptide after laser treatment. We found that in the i.p. and intravitreal injection of rAPN resulted in 78% and 68% inhibition respectively in the size of CNV complex compared to control mice. Similar results were observed when APN peptide was injected intravitreally or i.p. Treatment with rAPN or the peptide resulted in decreased levels of vascular endothelial growth factor. Thus, APN inhibited choroidal angiogenesis and may have therapeutic implications in the treatment of wet age related macular degeneration.     

24S-hydroxycholesterol and cholesterol-24S-hydroxylase (CYP46A1) in the retina: from cholesterol homeostasis to pathophysiology of glaucoma

Free cholesterol is the predominant form of cholesterol in the neural retina. The vertebrate neural retina exhibits its own capacity to synthesize cholesterol and meets its demand also by taking it from the circulation. Defects in cholesterol synthesis and trafficking in the neural retina has detrimental consequences on its structure and function, highlighting the crucial importance of maintaining cholesterol homeostasis in the retina. Our purpose was to give a review on the functioning of the retina, the role of cholesterol and cholesterol metabolism therein, with special emphasis on cholesterol-24S-hydroxylase (CYP46A1). Similar to the brain, the retina expresses cholesterol-24S-hydroxylase (CYP46A1) and is enriched in its metabolic product, 24S-hydroxycholesterol. We recently published that one single nucleotide polymorphism in CYP46A1 gene, designated as rs754203, was a risk factor for glaucoma. Glaucoma is the second leading cause of blindness worldwide, affecting more than 60 million people. Glaucoma is characterized by the loss of retinal ganglion cells, which show high CYP46A1 expression. These data suggest the potential involvement of CYP46A1 and 24S-hydroxycholesterol in the pathophysiology of glaucoma.     

Zinc binding to the Tyr402 and His402 allotypes of complement factor H: possible implications for age-related macular degeneration

The Tyr402His polymorphism of complement factor H (FH) with 20 short complement regulator (SCR) domains is associated with age-related macular degeneration (AMD). How FH contributes to disease pathology is not clear. Both FH and high concentrations of zinc are found in drusen deposits, the key feature of AMD. Heterozygous FH is inhibited by zinc, which causes FH to aggregate. Here, zinc binding to homozygous FH was studied. By analytical ultracentrifugation, large amounts of oligomers were observed with both the native Tyr402 and the AMD-risk His402 homozygous allotypes of FH and both the recombinant SCR-6/8 allotypes with Tyr/His402. X-ray scattering also showed that both FH and SCR-6/8 allotypes strongly aggregated at > 10 μM zinc. The SCR-1/5 and SCR-16/20 fragments were less likely to bind zinc. These observations were supported by bioinformatics predictions. Starting from known zinc binding sites in crystal structures, we predicted 202 putative partial surface zinc binding sites in FH, most of which were in SCR-6. Metal site prediction web servers also suggested that SCR-6 and other domains bind zinc. Predicted SCR-6/8 dimer structures showed that zinc binding sites could be formed at the protein-protein interface that would lead to daisy-chained oligomers. It was concluded that zinc binds weakly to FH at multiple surface locations, most probably within the functionally important SCR-6/8 domains, and this explains why zinc inhibits FH activity. Given the high pathophysiological levels of bioavailable zinc present in subretinal deposits, we discuss how zinc binding to FH may contribute to deposit formation and inflammation associated with AMD.     

Microbial diversity in acid mineral bioleaching systems of dongxiang copper mine and Yinshan lead–zinc mine

To understand the composition and structure of microbial communities in acid mineral bioleaching systems, the molecular diversity of 16S rDNA genes was examined using a PCR-based cloning approach. A total of 31 Operational Taxonomic Units (OTUs) were obtained from the four samples taken from four different bioleaching sites in Yinshan lead–zinc mine and Dongxiang copper mine in Jiangxi Province, China. The percentages of overlapping OTUs between sites ranged from 22.2 to 50.0%. Phylogenetic analysis revealed that the bacteria present at the four bioleaching sites fell into six divisions, α-Proteobacteria (1.1%), β-Proteobacteria (2.3%), γ-Proteobacteria (30.8%), Firmicutes (15.4%), Actinobacteria (0.3%) and Nitrospira (50.1%). Organisms of genera Leptospirillum, Acidithiobacillus, and Sulfobacillus, which were in Nitrospira, γ-Proteobacteria, and Firmicutes divisions, respectively, were the most dominant. The results of principal component analysis based on the six phylogenetic divisions and biogeochemical data indicated that the microbial community structure of a site was directly related to the biogeochemical characteristic of that site. It follows therefore that sites with similar biogeochemical characteristics were comprised of similar microbial community structures. The results in our study also suggest that the elements copper and arsenic appear to be the key factors affecting the compositions and structures of microbial community in the four bioleaching sites. Zhiguo He, Shengmu Xiao, Xuehui Xie are equally contributed to this work.