The effects of oxidative stress on the compressive damage thresholds of C2C12 mouse myoblasts: implications for deep tissue injury.

Abstract

Deep tissue injury (DTI) is a severe kind of pressure ulcers formed by sustained deformation of muscle tissues over bony prominences. As a major clinical issue, DTI affects people with physical disabilities, and is obviously related to the load-bearing capacity of muscle cells in various in vivo conditions. It has been hypothesized that oxidative stress, either induced by reperfusion immediately following tissue unloading or in chronic inflammatory conditions, may affect the cellular capacity against subsequent mechanical damages. In this study, we measured the compressive damage threshold of C2C12 mouse myoblasts with or without pre-treatment of hydrogen peroxide as an oxidative agent to understand how changes in the oxidative environment may contribute to the development of DTI. Spherical indentation was applied onto a layer of agarose gel (3 mm thick) covering a monolayer of C2C12 myoblasts. Cell damage was recognized by using a cell membrane damage assay, propidium iodide. The spatial profile of the measured percentage cell damage was correlated with the radially varying stress field as determined by finite element analysis to estimate the compressive stress threshold for cell damage. Results supported the hypothesis that chronic exposure to high-dosage oxidative stress could compromise the capability of muscle cells to withstand compressive damages, while short exposure to low-dosage oxidative stress could enhance such capability.