Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells.

Prolonged antibiotic treatment can lead to detrimental side effects in patients, including ototoxicity, nephrotoxicity, and tendinopathy, yet the mechanisms underlying the effects of antibiotics in mammalian systems remain unclear. It has been suggested that bactericidal antibiotics induce the formation of toxic reactive oxygen species (ROS) in bacteria. We show that clinically relevant doses of bactericidal antibiotics-quinolones, aminoglycosides, and β-lactams-cause mitochondrial dysfunction and ROS overproduction in mammalian cells.

Porcine intact and wounded skin responses to atmospheric nonthermal plasma.

Thermal plasma is a valued tool in surgery for its coagulative and ablative properties. We suggested through in vitro studies that nonthermal plasma can sterilize tissues, inactive pathogens, promote coagulation, and potentiate wound healing. The present research was undertaken to study acute toxicity in porcine skin tissues.

Effects of non-thermal plasma on mammalian cells.

Thermal plasmas and lasers have been widely used in medicine to cut, ablate and cauterize tissues through heating; in contrast, non-thermal plasma produces no heat, so its effects can be selective. In order to exploit the potential for clinical applications, including wound healing, sterilization, blood coagulation, and cancer treatment, a mechanistic understanding of the interaction of non-thermal plasma with living tissues is required. Using mammalian cells in culture, it is shown here that non-thermal plasma created by dielectric barrier discharge (DBD) has dose-dependent effects that range from increasing cell proliferation to inducing apoptosis.

Non-thermal plasma induces apoptosis in melanoma cells via production of intracellular reactive oxygen species.

Non-thermal atmospheric pressure dielectric barrier discharge (DBD) plasma may provide a novel approach to treat malignancies via induction of apoptosis. The purpose of this study was to evaluate the potential of DBD plasma to induce apoptosis in melanoma cells. Melanoma cells were exposed to plasma at doses that did not induce necrosis, and cell viability and apoptotic activity were evaluated by Trypan blue exclusion test, Annexin-V/PI staining, caspase-3 cleavage, and TUNEL® analysis.

Endothelial cell proliferation is enhanced by low dose non-thermal plasma through fibroblast growth factor-2 release.

Non-thermal dielectric barrier discharge plasma is being developed for a wide range of medical applications, including wound healing, blood coagulation, and malignant cell apoptosis. However, the effect of non-thermal plasma on the vasculature is unclear. Blood vessels are affected during plasma treatment of many tissues and may be an important potential target for clinical plasma therapy.

Cell proliferation following non-thermal plasma is related to reactive oxygen species induced fibroblast growth factor-2 release.

Non-thermal dielectric barrier discharge plasma is currently being developed for a wide range of medical applications, including blood coagulation, malignant cell apoptosis, and wound healing. However, the effect of non-thermal plasma on the vasculature is unclear. Blood vessels are affected during plasma treatment of many tissues, and vessels themselves may be an important clinical plasma therapy target.

Non-thermal dielectric barrier discharge plasma treatment of endothelial cells.

Non-thermal dielectric barrier discharge plasma is now being widely developed for various medical applications such as skin sterilization, blood coagulation, induction of apoptosis in malignant tissues, and wound healing among others. In this paper, we investigate the toxicity of non-thermal plasma treatment on endothelial cells, which line all blood contacting surfaces in the body. Our initial results indicate that low power non-thermal plasma is relatively non-toxic to endothelial cells at short exposure times up to 30 s, while non-thermal plasma treatment at longer exposure times is cytotoxic.