Do Antimonite and Silicon Share the Same Root Uptake Pathway by Lsi1 in L. Moench?

A study was conducted to further develop our understanding of antimony (Sb) uptake in plants. Unlike other metal(loid)s, such as silicon (Si), the mechanisms of Sb uptake are not well understood. However, SbIII is thought to enter the cell via aquaglyceroporins.

Multiple effects of silicon on alleviation of nickel toxicity in young maize roots.

Although beneficial metalloid silicon (Si) has been shown to alleviate the toxicity of various heavy metals, there is a lack of knowledge about the role of Si in possible alleviation of phytotoxicity caused by excess of essential nickel (Ni). In the present study we investigated the growth and biomass production, reactive oxygen species (ROS) formation and activities of selected antioxidants, as well as combined effect of Ni and Si on the integrity of cell membranes and electrolyte leakage in young maize roots treated for 24, 48 and 72 h with excess of Ni and/or Si. By histochemical methods we also visualized Ni distribution in root tissues and compared the uptake of Ni and Si with the development of root apoplasmic barriers.

Contrasting the roles of the I-II loop gating brake in CaV3.1 and CaV3.3 calcium channels.

Low-voltage-activated CaV3 channels are distinguished among other voltage-activated calcium channels by the most negative voltage activation threshold. The voltage dependence of current activation is virtually identical in all three CaV3 channels while the current kinetics of the CaV3.3 current is one order slower than that of the CaV3.

TGFβ1 downregulates neurite outgrowth, expression of Ca2+ transporters, and mitochondrial dynamics of in vitro cerebellar granule cells.

Acute injury to central nervous system (CNS) triggers neurodegenerative processes that can result in serious damage or complete loss of function. After injury, production of transforming growth factor β1 (TGFβ1) increases and initiates creation of a fibrotic scar that prevents normal growth, plasticity, and recovery of damaged neurons. Administration of TGFβ1 antagonists can prevent its pathological effects.