Long-term schisandrin B treatment mitigates age-related
impairments in mitochondrial antioxidant status and functional ability in
various tissues, and improves the survival of aging C57BL/6J mice
Issue title: Integrated Functions of Diet in Anti-Aging and
Cancer Prevention: Papers from the 4th International Niigata Symposium on Diet
and Health, 20–30 November 2008, Niigata, Japan
Affiliations: Department of Biochemistry, Hong Kong University of
Science & Technology, Hong Kong, China
Note: [] Address for correspondence: Dr. K.M. Ko, Department of
Biochemistry, Hong Kong University of Science & Technology, Clear Water
Bay, Hong Kong SAR China. Tel.: +852 2359 7298; Fax: +852 2358 1552; E-mail:
bcrko@ust.hk
Abstract: Mitochondrial decay is a major cause of aging, leading to the
subsequent death of aerobic organisms including humans. In the present study,
we examined the effects of supplementation with schisandrin B (Sch B, a
dibenzocyclooctadiene derivative isolated from the fruit of Schisandra
chinensis), administered at 0.012% (w/w) of diet, starting from the age of 36
weeks, on age-dependent changes in mouse mitochondrial antioxidant status and
functional ability in various tissues (brain, heart, liver, and kidney) up to
the age of 120 weeks. We also monitored survival of male and female C57BL/6J
mice. Aging caused progressive impairment in mitochondrial antioxidant status
in various tissues, as evidenced by decreases in reduced glutathione and
α-tocopherol levels, and Mn-superoxide dismutase activity. Impairments in
mitochondrial antioxidant status were invariably associated with increases in
mitochondria-driven reactive oxygen species (ROS) production in tissue
homogenates, as well as decreased mitochondrial ATP-generation capacities
(ATP-GCs), in all tested tissues. Diet supplementation with Sch B ameliorated
impairment in mitochondrial antioxidant status during aging. The effects were
more pronounced in younger than in older mice, when compared to age-matched
non-supplemented controls. Sch B supplementation also suppressed
mitochondria-driven ROS production and enhanced mitochondrial ATP-GC in various
tissues during aging. The beneficial effects of Sch B supplementation on
mitochondrial antioxidant status and functional ability were paralleled by
survival improvement in aging male mice, when compared with controls. Sch B
supplementation also improved the survival in female mice. In conclusion,
long-term Sch B supplementation mitigated age-dependent impairments in
mitochondrial antioxidant capacity and functional ability, thereby retarding
the aging process in mice, particularly during early aging.
