RESUMEN
The usual form of direct gastrointestinal injury following high-tension electric injury is widespread necrosis of the colon or the small intestine. It usually occurs in combination with extensive electric burns of the overlying abdominal wall. We report a case of immediate post-electrocution abdominal wall and stomach perforation following high tension electric injury. The total absence of coagulation necrosis of the stomach or other portions of the gastrointestinal tract and the absence of burns of the abdominal wall were other unique features of the case reported. The patient was successfully treated.
Asunto(s)
Músculos Abdominales/lesiones , Traumatismos por Electricidad , Estómago/lesiones , Adolescente , Traumatismos por Electricidad/diagnóstico , Traumatismos por Electricidad/terapia , Humanos , MasculinoRESUMEN
Lysosomal cathepsins have recently been reported to play crucial roles in the regulation of the mitochondrial death cascade by an unclear mechanism leading to mitochondrial membrane permeabilization. Glycosaminoglycans (GAG) are a family of ionic polysaccharides present at the lysosomal compartment and shown to inhibit lysosomal cathepsin activities. The implication of this family of polysaccharides in the regulation of the pre-mitochondrial death cascade has still not been considered. Here, we demonstrate in a model of skin fibroblasts submitted to oxidative stress that a GAG-mimetic protects the lysosome from membrane disruption, reduces intracellular ROS levels, and inhibits mitochondrial membrane potential collapse, cytochrome c release and caspases-9 and -3 activations without affecting the extrinsic pathway of apoptosis. Heparan sulfate and chondroitin sulfate, but not heparin, showed also protecting effects when assessing key points of the intrinsic pathway of apoptosis. We suggest the existence of molecular links between endogenous GAGs and the regulation of apoptosis.