Anti-aging potential: Aconitase-inducing ingredient protects mitochondria

Key Points

San Antonio - In laboratory testing, a new aconitase-inducing active ingredient (AC) has shown the ability to protect mitochondria under stressful circumstances, and, thus, possesses anti-aging and antioxidant potential, an expert says.

Among the enzymes required for mitochondrial activity, aconitase plays a crucial role in energy production and protection of mitochondrial DNA, according to says Nouha Domloge, M.D., a dermatologist who is research director of Vincience's ISP Global Skin Research Center in Sophia Antipolis, France.

Therefore, it helps prevent energy decline induced by oxygen radicals, Dr. Domloge said at the American Academy of Dermatology (AAD) 2008 Winter Meeting.

Researchers evaluated the impact of AC on aconitase activity, cell viability after different stresses, DNA protection and ATP level. For the aconitase activity test, researchers pretreated human fibroblasts with a solution containing 1 percent AC for 24 or 48 hours. Then they submitted the fibroblasts to stresses such as UVB (100 mJ/cm² ), H₂O₂ (5 mm for 30 minutes) or nitric oxide (NO) stress (0.5 mm for 24 or 48 hours).

In the UVB testing, pre-treatment with the active ingredient achieved a 56 percent increase in total aconitase activity (p=0.0485), and a 69 percent increase in aconitase activity in fibroblasts subjected to UVB stress and treated again with AC for 24 hours (p=0.0084).

Mitochondrial DNA showed similar increases, Dr. Domloge says.

In particular, total mitochondrial aconitase activity rose 32 percent (p=0.0012) after pretreatment with AC, and 67 percent (p=0.0353) in the fibroblasts exposed to UVB stress and re-treated for 24 hours afterward.

Additionally, comet assays performed on UVB-exposed fibroblasts revealed a significant decrease (25 percent, p=0.0261) in tail moment due to AC treatment.

Furthermore, a tetrazolium (MTT) assay revealed a 21 percent increase in cell viability (p=0.0027) in unstressed fibroblasts treated with AC.

Researchers also observed a significant increase in cell viability in treated cells after UVB and H₂O₂ exposure (plus 21 percent, p=0.00003; plus 25 percent, p=0.0093, respectively). Similarly, AC treatment significantly increased cellular energy assessed by ATP level (up 43 percent, p=0.0027 at one hour).

H&E staining of fibroblasts and ex vivo skin stressed with NO also revealed that AC treatment achieved improvements, Dr. Domloge says.

In the former area, AC-treated fibroblasts exhibited improvements in cellular morphology compared to untreated control fibroblasts.

In ex vivo skin testing, AC-treated samples showed a better preservation of epidermal structure than untreated controls. Similar results emerged from H₂O₂ testing of ex vivo skin.