イエウサギVX2移植舌癌に及ぼす superoxide dismutaseならびに peplomycinの影響に関する実験的研究

抄録

It has been recently suggested that active oxygen species such as superoxide (SO) have carcinogenic and anticancer effects. Anticancer agents such as peplomycin (PEP), which are widely used in the treatment of oral cancer, produce pulmonary fibrosis and other side effects which might be caused by SO. Superoxide dismutase (SOD) inactivates SO and protects against physical SO injury.
In order to investigate the effects of intravenous PEP and SOD, given singly or in combination, on VX2 carcinoma implanted in the tongue and pulmonary tissue of domestic rabbits, light and electron microscopic studies were performed. The preventive effect of these drugs on lymph node metastasis was determined by histopathological investigation of the positive rate of metastasis (PRM). In addition, the collagen content in the pulmonary tissues and the oxygen partial pressure of arterial blood (P_aO₂) in the left ventricle were measured.
The following results were obtained:
1. Anticancer effects on VX2 carcinoma implanted in the tongue were recognized in the PEP and PEP-SOD groups. The values of PRM in the cervical lymph nodes and lung in the PEP and PEPSOD groups were significantly lower than those of the SOD and control groups.
2. Electron microscopic examination of VX2 carcinoma cells of the tongue in the PEP and PEPSOD groups showed pycnosis, karyorrhexis, vacuolization and indistinct cell borders. Electron microscopic examination of the pulmonary tissue in the PEP groups showed increased fibroblasts and collagen fibers in the alveolar walls. In the PEP-SOD groups, there were far less inflammatory changes and significantly milder pulmonary fibrosis.
3. The collagen content in the PEP-SOD groups was lower than that in the PEP groups.
4. The P_aO₂ of the left ventricle in the PEP-SOD groups was higher than that in the PEP groups.
These findings indicated that the use of SOD concurrently with PEP in the chemotherapy of oral cancer, inhibited the induction of pulmonary fibrosis associated with PEP withoutaffecting the anticancer effect of this agent.