Systemic toxicity induced by paclitaxel in vivo is associated with the solvent cremophor EL through oxidative stress-driven mechanisms.

Highlights: [•] Our data indicate the existence of a continuous oxidative stress generation during in vivo cremophor-paclitaxel treatment. [•] CREL is primarily responsible for the in vivo oxidative damage of PTX formulation on erythrocytes. [•] PTX affects the systemic oxidative profile primarily by impairing the antioxidant defenses. [ABSTRACT FROM AUTHOR]