Docosahexaenoic acid inhibits melanin synthesis in murine melanoma cells in vitro through increasing tyrosinase degradation
Abstract
Marie Carmel BALCOS1, Su Yeon KIM1, Hyo-soon JEONG1, Hye-young YUN1, Kwang Jin BAEK1, Nyoun Soo KWON1, Kyoung-chan PARK2, Dong-seok KIM1, *
1Department of Biochemistry, Chung-Ang University College of Medicine, 221 Heukseok-dong, Dongjak-gu, Seoul 156–756, Korea; 2Department of Dermatology, Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-si, Kyoungki-do 463–707, Korea
Aim: To investigate the effects of docosahexaenoic acid (DHA) on melanin synthesis and related regulatory mechanisms.
Methods: B16F10 mouse melanoma cells were exposed to DHA for 3 d, and melanin content and tyrosinase activity were measured. Western blot analysis was used to analyze the protein levels in DHA-mediated signal transduction pathways.
Results: DHA (1–25 μmol/L) did not affect the viability of B16F10 cells, but decreased α-MSH-induced melanin synthesis in a concentration-dependent manner. DHA concentration-dependently reduced tyrosinase activity in the cells, but did not affect mushroom tyrosinase activity in a cell-free system. Furthermore, DHA treatment significantly reduced tyrosinase level without affecting microphthalmia-associated transcription factor (MITF) in the cells. DHA did not activate ERK and Akt in the cells. Pretreatment with the proteasome inhibitor MG132 (80 nmol/L) abolished DHA-induced tyrosinase reduction.
Conclusion: DHA inhibits melanogenesis in B16F10 cells in vitro through increasing tyrosinase degradation. The results suggest that DHA may be a potential agent for treatment of hyperpigmentary disorders of skin.
Keywords: docosahexaenoic acid; α-MSH; melanin; melanogenesis; tyrosinase; proteasome; MG132; skin; hyperpigmentary disorders
The studies were mainly supported by research grants from the National Natural Science Foundation of China (81073090 and 81274134). We thank Prof Hou-kai LI (Shanghai University of Traditional Chinese Medicine) for his contribution to the English translation.
* To whom correspondence should be addressed.
E-mail ds_kim@cau.ac.kr
Received 2013-05-15 Accepted 2013-11-11
Keywords:
1Department of Biochemistry, Chung-Ang University College of Medicine, 221 Heukseok-dong, Dongjak-gu, Seoul 156–756, Korea; 2Department of Dermatology, Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-si, Kyoungki-do 463–707, Korea
Aim: To investigate the effects of docosahexaenoic acid (DHA) on melanin synthesis and related regulatory mechanisms.
Methods: B16F10 mouse melanoma cells were exposed to DHA for 3 d, and melanin content and tyrosinase activity were measured. Western blot analysis was used to analyze the protein levels in DHA-mediated signal transduction pathways.
Results: DHA (1–25 μmol/L) did not affect the viability of B16F10 cells, but decreased α-MSH-induced melanin synthesis in a concentration-dependent manner. DHA concentration-dependently reduced tyrosinase activity in the cells, but did not affect mushroom tyrosinase activity in a cell-free system. Furthermore, DHA treatment significantly reduced tyrosinase level without affecting microphthalmia-associated transcription factor (MITF) in the cells. DHA did not activate ERK and Akt in the cells. Pretreatment with the proteasome inhibitor MG132 (80 nmol/L) abolished DHA-induced tyrosinase reduction.
Conclusion: DHA inhibits melanogenesis in B16F10 cells in vitro through increasing tyrosinase degradation. The results suggest that DHA may be a potential agent for treatment of hyperpigmentary disorders of skin.
Keywords: docosahexaenoic acid; α-MSH; melanin; melanogenesis; tyrosinase; proteasome; MG132; skin; hyperpigmentary disorders
The studies were mainly supported by research grants from the National Natural Science Foundation of China (81073090 and 81274134). We thank Prof Hou-kai LI (Shanghai University of Traditional Chinese Medicine) for his contribution to the English translation.
* To whom correspondence should be addressed.
E-mail ds_kim@cau.ac.kr
Received 2013-05-15 Accepted 2013-11-11