Current status of calcium in hepatocellular injury

A major question being addressed in hepatocellular injury is whether a unifying mechanism exists which involves a loss of regulation of cellular Ca++ levels. In this regard, alterations of Ca++ homeostasis have been proposed to play a major role in cell injury induced by a diversity of situations such as chemical intoxication and abnormal physiological states such as ischemia. In this review, we will discuss some of the available literature concerning hepatocellular Ca++ homeostasis, means by which it can be disrupted and how such disruptions may lead to loss of cell viability. Recent studies suggest that the ability of certain pathological conditions to intensify hepatocellular damage appears to be related to activation of molecular oxygen, a process termed oxidative stress (1, 2). We will present evidence which highlights the complex interrelationship between Ca++ homeostasis and oxidative stress in cell injury. In spite of intensive research effort, a complete understanding of the events resulting in a perturbation of Ca++ homeostasis, and its consequences, remains elusive. It is apparent that much more information concerning the effects of pathological conditions on the distribution and functions of Ca++ in the liver and its various cell types is needed.