Contribution to understanding the influence of fires on the mercury cycle: Systematic review, dynamic modelling and application to sustainable hypothetical scenarios.

Mercury (Hg) mobilization and accumulation in the environment is directly related to forest fires. Biomass burning accounts for about 13% of the total contribution of Hg from natural sources. The aim of this work is to contribute to the knowledge of how wildfires modify mercury compounds behaviour and the effects it has in the Hg cycle, based on a systematic bibliographic review and analysis. Systems dynamics is an adequate focus to analyze the mobilization of Hg due to wildfires, which meets all the requirements to be studied by multimedia modelling. The development and application for the first time of a dynamic multimedia model of Hg taking into account specifically the influences of wildfires is one of the novelties of this work. Different scenarios show that an increase in the number of fires will consequently increase the mercury emitted into the atmosphere, modifying its natural cycle, producing a long-term modification of Hg compositions and concentrations in the different media. Hg movement caused by wildfires can cause complications in living beings and alter the ecosystems. This study found that the Hg soil content could as well be an indicator to measure the impact of fire on the environment. This model can also be generalized to conduct additional studies under comparable conditions, helping to understand the importance of forest fires in global Hg cycles.

A Novel HDL-Mimetic Peptide HM-10/10 Protects RPE and Photoreceptors in Murine Models of Retinal Degeneration.

Age-related macular degeneration (AMD) is a leading cause of blindness in the developed world. The retinal pigment epithelium (RPE) is a critical site of pathology in AMD. Oxidative stress plays a key role in the development of AMD. We generated a chimeric high-density lipoprotein (HDL), mimetic peptide named HM-10/10, with anti-oxidant properties and investigated its potential for the treatment of retinal disease using cell culture and animal models of RPE and photoreceptor (PR) degeneration. Treatment with HM-10/10 peptide prevented human fetal RPE cell death caused by tert-Butyl hydroperoxide (tBH)-induced oxidative stress and sodium iodate (NaIO3), which causes RPE atrophy and is a model of geographic atrophy in mice. We also show that HM-10/10 peptide ameliorated photoreceptor cell death and significantly improved retinal function in a mouse model of N-methyl-N-nitrosourea (MNU)-induced PR degeneration. Our results demonstrate that HM-10/10 protects RPE and retina from oxidant injury and can serve as a potential therapeutic agent for the treatment of retinal degeneration.