Influences of chronic tobacco smoke inhalation on aging and oxidant-antioxidant balance in the senescence-accelerated mouse (SAM)-P/2.

We studied the influences of chronic tobacco exposure on aging and oxidant-antioxidant balance in two different strains of mice, hitherto called SAM (senescence-accelerated mice). One is a senescence-prone strain, "SAM-P/2," and another is a senescence-resistant strain, "SAM-R/1." We used 100 male mice--20 young (12 weeks of age) mice and 30 mature (24 weeks of age) mice from each strain. Half of each series were housed in a Hamburg II machine and exposed to tobacco smoke inhalation for five weeks. The result was that fewer of the mature SAM-P/2 survived compared with the mature SAM-R/1 after chronic tobacco inhalation. The grading of senility in the mature SAM-P/2 was also significantly higher than that in the mature SAM-R/1. The reduction of glutathione contents of blood and liver after tobacco exposure in the mature SAM-P/2 was greater than that in the young SAM-P/2 and the mature SAM-R/1. Moreover, oxygen radical generation of total blood cells stimulated by phorbol-myristate-acetate or opsonized zymosan showed a greater increase in the mature SAM-P/2 compared to the young SAM-P/2 and the mature SAM-R/1. These results indicate that the senescence-prone strain (SAM-P/2) was more susceptible to tobacco smoke exposure than the resistant strain (SAM-R/1). The impaired oxidant-antioxidant balance in the SAM-P/2 may therefore contribute to the process of senescence acceleration.