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Symmetry-based explanations using symmetry breaking (SB) as the key explanatory tool have complemented and replaced traditional causal explanations in various domains of physics. The process of spontaneous SB is now a mainstay of contemporary explanatory accounts of large chunks of condensed matter physics, quantum field theory, nonlinear dynamics, cosmology, and other disciplines. A wide range of empirical research into various phenomena related to symmetries and SB across biological scales has accumulated as well. Led by these results, we identify and explain some common features of the emergence, propagation, and cascading of SB-induced layers across the biosphere. These features are predicated on the thermodynamic openness and intrinsic functional incompleteness of the systems at stake and have not been systematically analyzed from a general philosophical and methodological perspective. We also consider possible continuity of SB across the physical and biological world and discuss the connection between Darwinism and SB-based analysis of the biosphere and its history.

Symmetry-based explanations using symmetry breaking (SB) as the key explanatory tool have complemented and replaced traditional causal explanations in various domains of physics. The process of spontaneous SB is now a mainstay of contemporary explanatory accounts of large chunks of condensed-matter physics, quantum field theory, nonlinear dynamics, cosmology, and other disciplines. A wide range of empirical research into various phenomena related to symmetries and SB across biological scales has accumulated as well. Led by these results, we identify and explain some common features of the emergence, propagation, and cascading of SB-induced layers across the biosphere. These features are predicated on the thermodynamic openness and intrinsic functional incompleteness of the systems at stake and have not been systematically analyzed from a general philosophical and methodological perspective. We also consider possible continuity of SB across the physical and biological world and discuss the connection between Darwinism and SB-based analysis of the biosphere and its history.

Увод. Познато је да астроцити преживљавају дуже излагања депривацији кисеоника и глукозе (OGD) и да преживљавају данима без нутријената у поређењу са изразито осетљивим неуронима. Разлози овако смањене осетљивости астроцита и даље нису довољно разјашњени. Шта више, промене мембранског потенцијала митохондрија (ψm) астроцита, као индикатора ћелијског енергетског метаболизма и вијабилности, нису испитане током симулиране реперфузије након дужег излагања OGD (односно 1 % О2 без глукозе у присуству ограничене количине алтернативних нутријената). Смањена осетљивост астроцита може бити последица коришћења алтернативних ванћелијских извора енергије, као и унутарћелијских залиха енергије у циљу одржања мембранског потенцијала митохондрија. Стратегија преживљавања астроцита током таквих метаболичких изазова и даље није јасна. Методе. У овој студији, култура астроцита изложена је депривацији глукозе (GD), OGD и њиховој сукцесивној комбинацији различитих трајања. Промене ψm, праћене путем промена у флуоресценцији JC-1, испитане су у току једног сата током симулиране реперфузије у циљу моделовања услова in vivo. Флуоресцентни обележивач митохондрија JC-1 улази у матрикс митохондрије у зависности од потенцијала мембране митохондрије, померајући при томе максимум флуоресценције из зеленог у црвени део спектра. Такође, ефекти фармаколошке инхибиције два битна метаболичка пута: аутофагије хлорокином (CQ) и липолизе орлистатом, испитани су током депривације нутријената. Праћен је утицај поменутих инхибиција на промене вијабилности астроцита бојењима са акридин наранџастим (AO) и пропидијум јодидом (PI), као и промене мембранског потенцијала митохондрија (JC-1). Резултати. Показали смо да су астроцити отпорни на дуже периоде OGD (у трајању од 6 и 8 часова) која је имала слаб утицај на ψm током симулиране реперфузије, док је GD довела до хиперполаризације мембранског потенцијала митохондрија астроцита..., Introduction. Astrocytes are known to tolerate long periods of oxygen-glucose deprivation (OGD) and they survive nutrient deprivation (ND) for days as compared to rather vulnerable neurons. The reasons for this reduced vulnerability of astrocytes are not well understood. In fact, changes in mitochondrial membrane potential (ψm), as the indicator of the cellular energy metabolism and viability, have not been investigated during simulated reperfusion after extended OGD exposure (i.e. 1 % of О2 without glucose in the presence of limited alternative nutrients). This reduced vulnerability could be due to utilization of the alternative extracellular sources of energy, as well as utilization of the internal energy stores, in maintenance of mitochondrial membrane potential. The pro-survival strategy of astrocytes under such metabolic challenge is still not clear. Methods. Here, we subjected astrocytes in culture to glucose deprivation (GD), OGD and combinations of both conditions varying in duration and sequence. Changes in ψm, visualized by the change in the fluorescence of JC-1, were investigated within one hour after reconstitution of oxygen and glucose supply, intended to model in vivo reperfusion. Fluorescent probe JC-1 enters the mitochondrial matrix in a potential-dependent manner, thus shifting its emission from green to red. Furthermore, the effects of inhibition of two potential steps in energy acquisition during ND: autophagy using chloroqione (CQ) and lipolysis using orlistat were investigated. Changes in astrocytes viability were followed with acridine orange (AO) and propidium iodide (PI) staining, and ψm was followed with JC-1. Results. We showed that astrocytes were resilient to extended periods of OGD (6 and 8 h), which had little effect on ψm during reperfusion, whereas GD contributed to a more negative ψm. Subsequent chemical oxygen deprivation induced by sodium azide caused depolarization, which, however, was significantly delayed as compared to the norm