“Systemic apoptotic response” after thermal burns

Abstract

The systemic pathophysiologic changes following thermal injuries affect multiple organs and body systems leading to clinical manifestations including shock, intestinal alterations, respiratory and renal failure, immunosuppression and others. Recent advances in the comprehension of mechanisms underlying systemic complications of thermal injuries have contributed to uncover part of the cellular and molecular basis that underlie such changes. Recently, programmed cell death (apoptosis) has been considered playing an important role in the development of such pathological events. Therefore, investigators utilizing animal models and clinical studies involving human primates have produced a large body of information suggesting that apoptosis is associated with most of the tissue damages triggered by severe thermal injuries. In order to draw the attention on the important role of apoptosis on systemic complications of thermal injuries, in this review we describe most of these studies, discuss possible cellular and molecular mechanisms and indicate ways to utilize them for the development of therapeutic strategies by which apoptosis may be prevented or counteracted.

Effective melatonin protection of burn-induced hepatic disorders in rats

“…Melatonin protects against burn-induced liver injury by scavenging the ROS and RNS, thereby preventing depletion of antioxidant capacity, inhibiting lipid peroxidation and releasing inflammatory mediators [19]. Melatonin also stabilizes cell membranes, making them more resistant to oxidative attacks [5].…”

“…Oxidative stress and lipid peroxidative damage of mitochondrial membranes trigger mitochondrial permeability and mitochondrial dysfunction, with resultant depletion of ATP and glutathione, and cell death [19]. Recently, apoptosis has found to be an important factor in pathological changes in the liver that occur after burns.…”

“…In the present study, melatonin, in the same dose, inhibited lipid peroxidation, degeneration and formation of apoptotic bodies (Councilman's bodies) in rat livers in the early post-burn period. Clinical investigations have shown that burninduced hepatic injury is accompanied by impairment of liver function [11,19]. Our previous data indicated that melatonin (10 mg/kg b.w.)…”

Captopril protects against burn-induced cardiopulmonary injury in rats

“…After thermal injuries, nearly every organ or tissue seems affected and manifests this peculiar cellular mechanism characterizing a "systemic apoptotic response". [49] Currently, ROS may mediate apoptosis through the starting of poly (ADPribose) polymerase (PARP), advances in mitochondrial permeability with the release of cytochrome C, and activation of caspases. [50,51] ROS-triggered release of lysosomal ingredients can also lead to apoptosis.…”

Melatonin protection against burn-induced liver injury. A review

“…Apoptosis of hepatocytes and endothelial cells is considered important in pathological hepatic changes and is a result of systemic apoptotic response occurring after burns [43]. Apoptosis plays an important role in inflammatory responses.…”