Abstract
We have investigated basic and clinical aspects of the melanogenesis inhibitory action of Kojic Acid (KA). Isolated tyrosinase activity obtained from mouse B-16 melanoma cells has been inhibited by KA dose dependently. KA has been found to inhibit melanin polymer formation through the dihydroxyindole (DHI) metabolic pathway from dopachrome by directly forming an intermediate through reaction with DHI.
The addition of 2.5mM KA to cultured B-16 cells induced whitening of cells accompanied with decreased tyrosinase activities. This has been found to be a reversible process and the B-16 cells can recover their tyrosinase activity and melanin forming ability after culturing in fresh KA free culture medium.
Concerning in vivo effect, addition of 0.15% KA into the fish-tank of Black Moor goldfish induced decrease of melanin pigmentation and converted the color of their integument from black to yellowish-light brown in 54 days. Furthermore, 1%-5% KA propylene glycol-ethanol solution dose dependently inhibited UV-induced pigmentation in brown guinea pigs. We then tested 31 male and 46 female volunteers with UV-induced hyper-pigmentation on the flexor surface of upper arm. Three applications of 1% KA cream per day for 21 days exhibited apparent suppression of UV-induced pigmentation in 90.3% of the males and 75.5% of the females.
On the basis of the above investigative studies, we have made clinical studies using 1% and 2.5% KA cream on chloasma, solar and senile lentigo as well as post-inflammatory hyper-pigmentation and ephelides. We have applied KA cream for more than 2 months in a total of 204 cases and evaluated its therapeutic effectiveness. Among these, 93 cases (45.6%) showed “markedly” or “moderately effective” results; 151 cases (74%) showed more than “slightly effective.” There is no distinct difference between 1% and 2.5% KA cream as to its clinical effectiveness in suppressing hyper-pigmentation.
