Effect of Temperature and Exposure Time on Cambium Cell Viability In Vitro for Eucalyptus Species

Research Highlights: Thermal damage to cambium cells of Eucalyptus held in vitro was recorded at sublethal temperatures (40 °C–50 °C) when the duration of exposure extends beyond 2.5 min up to 5 min. (2) Background and Objectives: During a forest fire, heat can be transferred through tree bark potentially impacting viability of vascular cambium cells and the perennial growth of the tree. With the increased temperature of the cambium, cells are known to lose viability at temperatures exceeding 60 °C. However, it is possible that extended exposure to temperatures below 60 °C may also impair cell viability. This study aimed to identify the effect of the temperature and exposure time interaction on the cambium cell viability of Eucalyptus, a genus widely distributed in natural forests and commercial plantations globally. (3) Methods: Excised cambium-phloem tissue sections from three Eucalyptus species (Messmate–E. obliqua L’Hér., Narrow-leaf peppermint–E. radiata Sieber ex DC. and Swamp gum–E. ovata Labill.) were exposed in vitro to a series of temperature–time treatments (40 °C, 50 °C, 60 °C, 70 °C for 1 min, 2.5 min, and 5 min) and tested for cell viability using a tetrazolium reduction method. (4) Results: Cell viability of cambium cells decreased with increased temperature and exposure times for all three Eucalyptus species. Longer exposure to sublethal temperatures of 40 °C to 50 °C showed statistically similar results to shorter exposure to lethal temperatures (>50 °C). (5) Conclusions: Longer exposure to sublethal temperatures (40 °C–50 °C) caused irreversible thermal damage to cambium cells of Eucalyptus when tested in vitro, further refining our understanding of raised temperature on cell viability

Cholesterol is necessary both for the toxic effect of Aβ peptides on vascular smooth muscle cells and for Aβ binding to vascular smooth muscle cell membranes

Accumulation of beta amyloid (Aâ) in the brain is central to the pathogenesis of Alzheimer's disease. Aâ can bind to membrane lipids and this binding may have detrimental effects on cell function. In this study, surface plasmon resonance technology was used to study Aâ binding to membranes. Aâ peptides bound to synthetic lipid mixtures and to an intact plasma membrane preparation isolated from vascular smooth muscle cells. Aâ peptides were also toxic to vascular smooth muscle cells. There was a good correlation between the toxic effect of Aâ peptides and their membrane binding. 'Ageing' the Aâ peptides by incubation for 5 days increased the proportion of oligomeric species, and also increased toxicity and the amount of binding to lipids. The toxicities of various Aâ analogs correlated with their lipid binding. Significantly, binding was influenced by the concentration of cholesterol in the lipid mixture. Reduction of cholesterol in vascular smooth muscle cells not only reduced the binding of Aâ to purified plasma membrane preparations but also reduced Aâ toxicity. The results support the view that Aâ toxicity is a direct consequence of binding to lipids in the membrane. Reduction of membrane cholesterol using cholesterol-lowering drugs may be of therapeutic benefit because it reduces Aâ-membrane binding

Targeting voltage-gated calcium channels in neurological and psychiatric diseases

Voltage-gated calcium channels are important regulators of brain, heart and muscle functions, and their dysfunction can give rise to pathophysiological conditions ranging from cardiovascular disorders to neurological and psychiatric conditions such as epilepsy, pain and autism. In the nervous system, calcium channel blockers have been used successfully to treat absence seizures, and are emerging as potential therapeutic avenues for pathologies such as pain, Parkinson disease, addiction and anxiety. This Review provides an overview of calcium channels as drug targets for nervous system disorders, and discusses potential challenges and opportunities for the development of new clinically effective calcium channel inhibitors