Coenzyme Q10--a therapeutic agent.

Coenzyme Q10 (CoQ10) is critical to production of adenosine triphosphate and is an antioxidant that scavenges reactive oxygen species during oxidative stress. The use of CoQ10 in treating oxidative stress in cardiovascular diseases, diabetes, and cancer is reviewed.

Coenzyme Q10 does not protect cochlear hair cells from death in the ischemic organotypic culture.

OBJECTIVE: To evaluate in vitro the effect of coenzyme Q10 (CoQ(10)) on ischemia-induced hair cell death. STUDY DESIGN: Organotypic cochlear cultures of newborn rats were subjected to ischemia with and without CoQ(10). RESULTS: Addition of CoQ(10) has not prevented HC loss. CONCLUSION: CoQ(10) seems to protect against only certain modes of cell death.

Anti-aging effects of co-enzyme Q10 on periodontal tissues.

Oxidative stress is associated with age-related reactions. The anti-oxidative effects of a reduced form of co-enzyme Q10 (rCoQ10) suppress oxidative stress, which may contribute to the prevention of age-related inflammatory reactions. We examined the effects of topically applied rCoQ10 on periodontal inflammatory reactions in a rat aging model. Male Fischer 344 rats, 2 (n = 6) and 4 mos (n = 18) of age, were used. All of the two-month-old rats and 6 of the four-month-old rats were sacrificed and 12 remaining four-month-old rats received topically applied ointment with or without 1% rCoQ10 on the gingival surface until they reached 6 mos of age. The rats showed an age-dependent increase in circulating oxidative stress. RCoQ10 decreased oxidative DNA damage and tartrate-resistant acid-phosphatase-positive osteoclasts in the periodontal tissue at 6 mos of age as compared with the control. The same conditions lowered gene expression of caspase-1 and interleukin-1ß in the periodontal tissue. Furthermore, Nod-like receptor protein 3 inflammasomes were less activated in periodontal tissues from rCoQ10-treated rats as compared with the control rats. Our results suggest that rCoQ10 suppresses age-related inflammatory reactions and osteoclast differentiation by inhibiting oxidative stress.

Coenzyme Q10 prevents human lens epithelial cells from light-induced apoptotic cell death by reducing oxidative stress and stabilizing BAX / Bcl-2 ratio.

BACKGROUND: Cataract is one of the most prevalent eye disease and a major cause for legal blindness in the world. Beside others, cumulative light-exposure and apoptotic cell death are significantly associated with cataract development. In contrast, supplementation with antioxidants has been suggested to prevent premature cataractogenesis. This study investigates possible protective effects of Coenzyme Q10 (CoQ10) regarding light-induced stress and apoptotic cell death in human lens epithelial cells (LEC). METHODS: Human LEC were either pre-incubated with CoQ10 or not and then exposed to white light. After 10-40 min of irradiation viability, induction of intracellular reactive oxygen species (ROS), apoptosis and cell death was determined. Expression of apoptotic BAX and anti-apoptotic Bcl-2 protein and their mRNA were determined by RT-PCR and Western blot analysis. RESULTS: Light exposure decreased LEC viability and Bcl-2 expression and increased intracellular ROS, apoptotic cell death, and BAX expression in a time-of-irradiation-dependent manner. Phototoxic cell death and apoptosis, as well as decrease of Bcl-2 and increase in BAX expression was significantly reduced, when cells were pre-incubated with CoQ10. CONCLUSIONS: In this study, CoQ10 significantly reduced light-induced LEC-damage and attenuated phototoxic effects on BAX and Bcl-2 expression. Therefore, CoQ10 supplementation might also be useful in preventing LEC death and consecutive cataract formation in vivo.

Effect of co-enzyme Q10 and alpha-lipoic acid on response of rabbit urinary bladder to repetitive stimulation and in vitro ischemia.

OBJECTIVES: To determine the efficacy of coenzyme Q10 (CoQ10) and alpha-lipoic acid (alpha-LA), either alone or in combination, to protect the contractile responses of the rabbit urinary bladder from damage caused by repetitive stimulation in the presence or absence of in vitro ischemia. METHODS: Four groups of New Zealand white rabbits (4 per group) were treated with vehicle (group 1), CoQ10 (group 2), alpha-LA (group 3), or CoQ10 plus alpha-LA (group 4) for 2 weeks. At the end of the treatment period, eight longitudinal strips from each rabbit bladder body were placed in oxygenated Tyrode's solution with glucose (normal physiologic medium). The strips were stimulated by field stimulation, carbachol, and KCl, and the responses were recorded. One half of the strips were switched for 1 hour to Tyrode's solution with no glucose equilibrated with nitrogen (ischemia medium). Simultaneously, all strips were subjected to 1 h of repetitive field stimulation followed by 1 hour of recovery in normal physiologic medium, and the responses to all stimuli were recorded again. RESULTS: CoQ10 showed no protective effect. Alpha-LA resulted in increased contractile responses of the control bladder and showed a moderate protective effect for all forms of stimulation. The combination, however, showed a significantly greater increase in the contraction of the control bladder and a greater protective effect than alpha-LA alone. CONCLUSIONS: The combination of alpha-LA and CoQ10 treatment enhanced the contractile response in normal medium and diminished the contractile dysfunction induced by repetitive field stimulation and ischemia.