Effects of low-intensity swimming on radiation-induced leg contracture in mice.

OBJECTIVE: To evaluate the effects of low-intensity swimming on radiation-induced leg contracture. METHODS: Forty mice were randomly and equally divided into four groups: 1) irradiation; 2) swimming before irradiation; 3) swimming after irradiation; 4) swimming after contracture, and their left hind legs were exposed to gamma irradiation of 60 Gy. The mice were allowed to swim freely for 10 minutes, three times per day. For group 2, the mice were allowed to swim for only 1 week before irradiation. For group 3, the mice were allowed to swim immediately after irradiation until day 130, post-irradiation. For group 4, the mice were allowed to swim after leg contracture happened (on day 30 post-irradiation) until day 130, post-irradiation. The leg lengths and knee joint angles were measured. Leg contracture was defined as the decrease in the hind leg lengths and the knee joint angles of each animal. The ultrastructural changes of gastrocnemius muscles were observed using transmission electron microscopy. RESULTS: The radiation could result in leg contracture and mitochondrial injury of the muscles. However, the group of swimming immediately after irradiation had less leg contracture and no vacuolar degeneration in the mitochondria, compared with the other groups. CONCLUSION: Low-intensity swimming that began immediately after the mice were irradiated could effectively prevent the irradiated legs from contracture. Patients with irradiated mastication muscles were recommended to begin mouth-opening exercises immediately after radiotherapy.

The effect of soft X-radiation on myofibrils.

Myofibrils, the contractile organelles from striated muscles, have been examined in the X-ray microscope to determine the effect of radiation on their function and structure. Using X-rays of energy 350-385 eV in the water window we find that after an exposure to 7.5 x 10(5) photons/micron2 (calculated to give an absorbed dose of 20,000 Gy) the myofibrils will no longer contract. The use of the free radical scavenging agent, DMSO, gives some protection to the fibrils. It has also been found that after this much irradiation the fibrils lose up to 20% of their mass. Further substantial mass loss occurs on subsequent irradiation. After 25 times the loss-of-function exposure only 30% of the mass remains. Analysis of a series of images of the same myofibril covering this range of exposures shows that the mass is preferentially lost in some areas of the structure and consequently significant structural changes occur.

Modification of myofibrils by fluorophore-induced photo-oxidation.

The excitation of fluorophores in the vicinity of a myofibril stops both shortening in the presence of ATP and Ca2+, and the extraction of the A-band by NaCl in the presence of Mg pyrophosphate. Shortening is more quickly affected than extraction. These effects can be induced by fluorescently-tagged antibodies bound in the A-band. Both depolymerization of the thick filament and the interaction between the myosin head and actin appear to be modified. Enzymatic lowering of the oxygen concentration in the bathing solution during excitation reduces these effects, indicating that they are due to photo-oxidation catalysed by excitation of the fluorophore. The results suggest that care needs to be exercised to minimize the consequences of these changes on the outcome of fluorescence-based assays of activity. Irradiated myofibrils that do not shorten, hydrolyse ATP at a rate comparable to those that contract, so they may be useful as a model system for the study of crossbridge activity in the ordered array of proteins of the myofibril.

Irradiations of rabbit myofibrils with an ultraviolet microbeam. I. Effects of ultraviolet light on the myofibril components necessary for contraction.

Glycerinated rabbit psoas myofibrils, F-actin, and myofibril ghosts were irradiated with ultraviolet light (UV) to investigate how UV blocks myofibril contraction. Myofibril contraction is most sensitive to 270- and 290-nm wavelength light. We irradiated I and A bands separately with 270- and 290-nm wavelength light using a UV microbeam and constructed dose-response curves for blocking sarcomere contraction. For both wavelengths, irradiations of A bands required less energy per area to block contraction than did irradiations of I bands, suggesting that the primary effects of both 270- and 290-nm wavelength light in stopping myofibril contraction are on myosin. We investigated whether the primary effect of UV in blocking I-band contraction is the depolymerization of actin by comparing the relative sensitivities of I-band contraction, F-actin depolymerization, and thin filament depolymerization to 270- and 290-nm light. We also compared the dose of UV required to depolymerize F-actin in solution with the dose needed to block I-band contraction and the dose required to alter thin filament structure in myofibril ghosts. The results confirm that UV blocks I-band contraction by depolymerizing actin. We discuss how the results might be relevant to the hypothesis that an actomyosin-based system is involved in chromosome movement.