Nitric oxide NO is synthesized

Nitric oxide (NO) is synthesized by conversion of the l-arginine to NO and l-citrulline through reaction which is catalyzed by nitric oxide synthetase (NOS) (Knowles and Moncada, 1994). NO as an important molecule not only play a role as second messenger but also binds to cytochrome c oxidase and decrease its affinity to oxygen. Binding of NO to cytochrome c oxidase affects ATP production and electron flux (Moncada and Bolaños, 2006). In addition, inhibiting the respiratory chain by NO elevates superoxide and hydrogen peroxide levels. In the high level the NO, superoxide is converted to peroxynitrite (ONOO−) rather than hydrogen peroxide (Poderos et al., 1998). So, excessive amount of NO contributes to neurological diseases (Dawson and Dawson, 1996). NO has ability to influence the function of respiratory chain and causes mitochondrial dysfunction. Incubation of the molar volume calculator mitochondria with ONOO− shows loss of activity in complex IV (Bolaños et al., 1995). Cardiolipin as the most abundant phospholipid in mitochondrial inner membrane, is peroxidized when complex IV loose its activity (Soussi et al., 1990). Moreover, exposure of the brain mitochondria to ONOO- decrease complex II activity as well (Brookes et al., 1998). NO prevents protein normal function and charcter through nitrosylation process. Sulfhydryls as main group of the active site in many enzymes are targeted by NO which changes protein function (Radi et al., 1991). Mitochondrial permeability transition pores (mPTPs) are channels in the contact site of the inner and outer membranes of the mitochondria. They are responsible for Ca hemostasis in non-pathological condition. But in the presence of the oxidative stress, ATP depletion and overloaded Ca opening of these channels releases pro-apoptotic proteins into the cytoplasm (Brenner and Grimm, 2006). ONOO- is one of the main molecules which can trigger mPTP opening under pathological conditions (Chavez et al., 1997). In AD, PD and HD peroxynitrite has crucial role through nitrosylation of proteins, opening of the mPTP and impairment of the mitochondrial activities especially electron transport chain (Asiimwe et al., 2016, Jiménez-Jiménez et al., 2016, Jamwal and Kumar, 2017). degraded mtDNA and low expression of complex I subunits are defined in early and definite AD brain specimens (Yan et al., 2013, Manczak et al., 2004). Complex II (succinate dehydrogenase (SDH) or succinate: ubiquinone oxidoreductase (SQR)) has 4 subunits which all of them are encoded by nuclear DNA. Studies showed mitochondrial complex II defect and lower activity in AD, PD and HD patients (Long et al., 2012, Hattori et al., 1991, Damiano et al., 2013). Complex III (Ubiquinol: cytochrome c oxidoreductase) has 11 subunits and one of them is encoded by mtDNA. In AD models this complex is inhibited by Aβ (Devi and Anandatheerthavarada, 2010). Recent studies showed that mutations in complex III subunits can be caused striatal atrophy in HD (Gu et al., 1996). Complex IV (cytochrome c oxidase) comprises 12 subunits that 3 of them are derived from mtDNA. α- synuclein as the main misfolded protein in PD can impair complex IV activity and function (Martin et al., 2006). In addition, previous studies showed platelets of PD patients had aberrations in complex IV activities (Benecke et al., 1993). in AD patients, Aβ inhibits activity of the cytochrome c oxidase as well as HD model (Casley et al., 2002, Tabrizi et al., 2000) (Fig. 1). Irregularities in activities of electron transport chain not only cause ROS generation but also show ATP depletion. Neurons depend on mitochondrial activites because of their high energy demand nature, for example activity of synapse needs to use high energy which is supplied by mitochondria (Jodeiri Farshbaf et al., 2016b).
Succinate dehydrogenase/succinate: ubiquinone oxidoreductase
Future direction
Conflict of interest
Introduction Greenhouse gases are chemical compounds, which induce the greenhouse effect. The rapidly increase in Earth’s atmospheric concentrations of the three main human-made greenhouse gases – carbon dioxide (CO2), methane (CH4), and nitrous oxide (NOx)– is clear from the data sets for these gases over the last 400,000 years. Among these greenhouse gasses, CO2 is the most important greenhouse gas produced by human activities, primarily through the combustion of fossil fuels. Its concentration in the Earth\'s atmosphere has risen by more than 30% since the Industrial Revolution. Thus, the development of technology for CO2 gas reduction drastically is important for the future. The first opportunity for CO2 gas reduction is the entry into force of the Kyoto Conference on Climate Change (COP3). The protocol concerning the reduction of CO2 in the atmosphere was deliberated at the COP3 [1]. Moreover, Paris climate accord is an agreement within the United Nations Framework Convention on Climate Change (UNFCCC) dealing with greenhouse gas emissions mitigation, adaptation and finance starting in the year 2020. The language of the agreement was negotiated by representatives of 196 parties at the 21st Conference of the Parties of the UNFCCC (COP21) in Paris and adopted by consensus on 12 December 2015 [2]. In order to implement the Paris climate accord, it is necessary to build a substantial CO2 reduction technology. Thus, the production of low-carbon fuels from CO2 by using renewable energy such as solar energy is important for mitigating global warming.