Cavitation damage to cellular membrane
Abstract
Despite the increasing concerns on traumatic injuries associated with shoulder-fired weapons in military sectors, rapid acceleration induced by such weapons has been exceedingly overlooked as possible injury mechanisms partially because overpressure is commonly regarded as a main cause. However, this projects preliminary studies using both pure water and tissue simulant (soft gels) have shown that seemingly small acceleration (~150g) triggers cavitation nucleation in the samples when their size is in the order of tens of centimeters. These experimental observations suggest that recoil energy of shoulder-fired weapons that apply up to 350g to a human body can result in large pressure in the shoulder areas or even inside a skull, which may trigger localized cavitation nucleation above a critical threshold. It is important to note that cells have hydrophobic cellular components, e.g., a nonpolar tail region in lipid bilayers. Such hydrophobic surfaces lower a critical threshold for cavitation nucleation and, as a result, will likely serve as cavitation nucleation sites when subjected to rapid acceleration (>150g). Cellular lipid bilayers, including a cell membrane and mitochondrial inner/outer membranes, play a very important role in activation/deactivation of regulatory pathways for cell injury and death. For example, it is well known that severe membrane damage could result in leakage of intracellular contents, influx of extracellular calcium ions, and subsequently irreversible cell death by necrosis. Similarly, damage to the mitochondrial membranes, e.g., mitochondrial permeability transition pore, may result in leakage of cytochrome complex that activates cell apoptosis.This projects main working hypothesis is that cellular lipid bilayer membranes, when subjected to >150g, are susceptible to cavitation-induced cell injuries from complete membrane disruption and irreversible cellular damage to partial membrane rupture and pore formation. The project aims to quantify cell death and injury as well as investigate the intimate link between the cell injury mechanisms and membrane permeability by developing and utilizing unique engineering solutions to biological challenges. Experimental characterization of impact and cell-death/-injury correlations at the cell population level and fundamental understanding of injury mechanisms at the single cell and subcellular level associated with military-relevant impact are essential for the development of reliable injury criteria, and more accurate prediction of injury that is specific to the characteristics of mechanical inputs. In addition, new findings on impact-induced cellular pathways that may trigger uncontrolled cell death, e.g., necrosis and apoptosis, could pave the way for innovative technical advances in the design of effective protective equipment, new biomedical technology for post-injury treatment, as well as new injury matrix a new matrix for better mitigation of the injury (e.g., timely rule changes among war fighters).
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- May 08, 2020
- Source ID
- N000142012409
Entities
People
- Wonmo Kang
Organizations
- Arizona State University
- Office of Naval Research
- United States Navy