Targeting mitochondrial impairment for the treatment of cardiovascular diseases: From hypertension to ischemia-reperfusion injury, searching for new pharmacological targets.

Mitochondria and mitochondrial proteins represent a group of promising pharmacological target candidates in the search of new molecular targets and drugs to counteract the onset of hypertension and more in general cardiovascular diseases (CVDs). Indeed, several mitochondrial pathways result impaired in CVDs, showing ATP depletion and ROS production as common traits of cardiac tissue degeneration. Thus, targeting mitochondrial dysfunction in cardiomyocytes can represent a successful strategy to prevent heart failure. In this context, the identification of new pharmacological targets among mitochondrial proteins paves the way for the design of new selective drugs. Thanks to the advances in omics approaches, to a greater availability of mitochondrial crystallized protein structures and to the development of new computational approaches for protein 3D-modelling and drug design, it is now possible to investigate in detail impaired mitochondrial pathways in CVDs. Furthermore, it is possible to design new powerful drugs able to hit the selected pharmacological targets in a highly selective way to rescue mitochondrial dysfunction and prevent cardiac tissue degeneration. The role of mitochondrial dysfunction in the onset of CVDs appears increasingly evident, as reflected by the impairment of proteins involved in lipid peroxidation, mitochondrial dynamics, respiratory chain complexes, and membrane polarization maintenance in CVD patients. Conversely, little is known about proteins responsible for the cross-talk between mitochondria and cytoplasm in cardiomyocytes. Mitochondrial transporters of the SLC25A family, in particular, are responsible for the translocation of nucleotides (e.g., ATP), amino acids (e.g., aspartate, glutamate, ornithine), organic acids (e.g. malate and 2-oxoglutarate), and other cofactors (e.g., inorganic phosphate, NAD+, FAD, carnitine, CoA derivatives) between the mitochondrial and cytosolic compartments. Thus, mitochondrial transporters play a key role in the mitochondria-cytosol cross-talk by leading metabolic pathways such as the malate/aspartate shuttle, the carnitine shuttle, the ATP export from mitochondria, and the regulation of permeability transition pore opening. Since all these pathways are crucial for maintaining healthy cardiomyocytes, mitochondrial carriers emerge as an interesting class of new possible pharmacological targets for CVD treatments.

Food waste composting - Is it really so simple as stated in scientific literature? - A case study.

Food waste has recently gained much worldwide interest due to its influence on the environment, economy and society. Gathering and recycling of food waste is the essential issue in the waste management and the interest in processing food waste arises mainly out of influence of the processes of food putrefaction on the environment. Composting of food waste encounters a number of technical challenges, arising weak physical structure of food waste with weak porosity, high content of water, low carbon-to-nitrogen relation and fast hydrolysis and accumulation of organic acids during composting. Therefore, the aim of this study was to investigate the challenges facing installations intended for food waste composting, with the purpose to their optimization with use of appropriate additives. Physico-chemical, biochemical characteristics and phytotoxicity of the produced compost has been measured. Two additives (20% biochar and 20% sawdust) were chosen from experimental variants I-XII containing different additives (biochar, Devonian sand, sawdust) in diverse concentration. The use of selected additives seems to slightly increase potential of hydrogen value and carbon-to-nitrogen ratio, while decreasing electrical conductivity in comparison with control sample. The results obtained also show that the addition of biochar leads to an increase dehydrogenase, phosphatase and arylsulphatase activities and addition of sawdust has a positive effect on beta-D-glucosidase, protease, phosphatase and arylsulphatase activities. The phytotoxicity test shows that the compost made of food waste (control sample) and with addition of biochar is toxic to plants. By contrast, the addition of sawdust shows that the compost was not phytotoxic. In conclusion, the addition of additives does not provide unambiguous results in terms of the quality of the final product in all monitored parameters. Therefore, we can state that food waste was reduced and hygienized, and that the final product does not meet conditions for mature compost.