Oxidant-induced lung injury in anticancer therapy.

Abstract Lung injury is one of the most frequent side effects in anticancer therapy. Especially simultaneous application of high doses of ionising radiation and radiosensitising cytotoxic drugs is considered to cause deleterious pneumonitis and pulmonary fibrosis. Growing evidence indicates that reactive oxygen species (ROS) play a key role in the development of these disorders. They are capable of causing cell component alterations and changing cellular protein expression. Observing these disease mechanisms reveals an impressive self-amplifying cascade of secondary ROS generation. Through intricate interactions between cells, cytokines and growth factors, fibroblasts are activated and thus pulmonary matrix content is massively increased. - As clinical appearance is uniform and unspecific, an early, reliable diagnosis of therapy-associated lung damage is not possible so far. However, improving this situation could enable us to take advantage of new multimodal therapeutic facilities. This review discusses mechanisms of ROS generation during radio-chemotherapy in the lung, antioxidant defense strategies and responses to oxidants, thereby assessing current diagnostic tools.