It has been shown to impair the normal proliferation of melanocytes through reactive oxygen species-dependent activation of GADD45.

[5] The compound can also be prepared by reducing raspberry ketone (4-(4-hydroxyphenyl)-2- butanone) with Raney nickel in EtOH.

This pathway involves reduction of the aliphatic double bond present in p-coumaric acid.

The mechanism of action of rhododendrol has been investigated in multiple studies which revealed that RD competes with tyrosine for hydroxylation by tyrosinase and interferes with melanin synthesis.

[2] However, another study stated that there was no ROS detected in the rhododendrol-treated melanocytes, but a tyrosinase-dependent accumulation of endoplasmic reticulum stress and activation of the apoptotic pathway.

Tyrosinase regularly plays an essential role in the production of melanocytes called the melanogenesis.

After oxidation of rhododendrol by the tyrosinase enzyme, several kinds of phenols and catechols are formed.

[2] Presence of o-quinones can lead to cytotoxicity via the production of reactive oxygen species (ROS) or by the binding to enzymes or DNA.

As described in the mechanisms of action, the presence of quinones could cause cytotoxicity to melanocytes by the production of ROS or by binding to DNA and enzymes.

[15] The study of Ito et al. showed that rhododendrol exerts its toxic effect in the melanocytes via tyrosinase-dependent mechanisms.

This tyrosinase enzyme breaks rhododendrol down into the following reactive metabolites: RD-quinone and RD-cyclic quinone.

[16] Auto-oxidation, in turn, causes oxidative stress to cells, which will impair the natural growth and function of the melanocytes.

Rhododenol and raspberry ketone impair the regular proliferation of melanocytes through reactive oxygen species-dependent activation of GADD45.

Also, the study of Abe et al. revealed that the autophagy pathway may be involved in the resistance to the cytotoxicity of RD.