In vivo demonstration of cytosolic calcium level shift by oxalates and cancer

Abstract

A series of experiments on the effects of oxalates on the dog’s heart sympathetic system resulted in the infiltration of calcium chelators into the adjacent atrial myocardium. The chelation process converts the ionic calcium into calcium carbonate (CaCO₃). We are presenting in vivo obtained images of the atrial myocyte cytoplasmic chelated calcium structures or mineralization. An increase of intracellular ionic calcium Ca⁺⁺ is known to trigger myocytes’ hypertrophy in transgenic mice. We are introducing a new in vivo approach that also changes intracellular ionic calcium stores. This change of the available cytoplasmic ionic calcium stores was accomplished via oxalate induced calcium chelation or sequestration. We demonstrate that the process of chelation causes an increase in the cytosolic Ca⁺⁺ level (a stress on the endoplasmic reticulum) which could affect the normal myocardial ionic cellular syncytial flow through gap junctions. Representative biopsied stained images via the von Kossa calcium specific technique are presented. The mineralized calcium stores are also seen physiologically coalescing against the intercalated disc. We discuss the role that the molecular size of the calcium salt plays on the interruption of normal syncytial flow through the gap junction, and the consequences of chelation on cell death.