The type and amount of melanin synthesized by the melanocyte, and its distribution pattern in the surrounding keratinocytes, determines the actual color of the skin. Melanin forms through a series of oxidative reactions involving the amino acid tyrosine in the presence of the enzyme tyrosinase. Tyrosinase catalyses three different reactions in the biosynthetic pathway of melanin in melanocytes: the hydroxylation of tyrosine to l-DOPA and the oxidation of l-DOPA to dopaquinone; furthermore, in humans, dopaquinone is converted by a series of complex reactions to melanin. Among the skin-lightening and depigmenting agents, magnesium-l-ascorbyl-2-phosphate (MAP), hydroxyanisole, N-acetyl-4-S-cysteaminylphenol, arbutin (hydroquinone-beta-d-glucopyranoside) and hydroquinone (HQ) are the most widely prescribed worldwide. However, with reports of potential mutagenicity and epidemics of ochronosis, there has been an increasing impetus to find alternative herbal and pharmaceutical depigmenting agents. A review of the literature reveals that numerous other depigmenting or skin-lightening agents are either in use or in investigational stages. Some of these, such as kojic, glycolic and azelaic acids, are well known to most dermatologists. Others have been discovered and reported in the literature more recently. Several depigmentation and lightening agents are discussed, including their historical background, biochemical characteristics, type of inhibition and activators from various sources. In addition, the clinical importance of mushroom tyrosinase as a recent prospect is discussed in this paper.

Tyrosinase is a copper-containing enzyme, which is widely distributed in microorganisms, animals and plants and is a key enzyme in melanin biosynthesis, involved in determining the color of mammalian skin and hair. In addition, unfavorable enzymatic browning of plant-derived foods by tyrosinase causes a decrease in nutritional quality and economic loss of food products. The inadequacy of current conventional methods to prevent tyrosinase action encourages researchers to seek new potent tyrosinase inhibitors for food and cosmetics. This article presents a study on the importance of tyrosinase, biochemical characteristics, type of inhibitions, activators from various natural sources with its clinical and industrial importance in recent prospects is discussed in this paper.

No abstract

It is known that reactive oxygen species (ROS) have a central role in causing many types of neuronal damage such as Alzheimer's disease, Parkinson's disease, ischemia, etc. 1,2)ROS comprise a group of unstable molecules: super oxide radical (O 2 Ϫ ), hydrogen peroxide (H 2 O 2 ), hydroxyl radical (OH) and hypochlorous acid (HOCl), that are generated in all cells as a by-product of cellular metabolism during conversion of molecular oxygen (O 2 ) to water (H 2 O). Additionally, phagocytes generate oxidative bursts of ROS to combat microorganisms. Cells possess endogenous systems (superoxide dismutase, catalase, glutathione peroxide) and diet derived (vitamin C and vitamin E) anti-oxidants to prevent or limit ROS induced tissue damage. H 2 O 2 is often used to investigate the mechanism of ROS-induced cell death, 3) and the mechanism of H 2 O 2 -induced PC12 cell death has been examined. 4,5) Hydroxyl radicals form when it comes in contact with a range of transition metal ions. Oxidative stress occurs during an imbalance between ROS and anti-oxidants. Excess production of ROS may lead to cellular injury through nonspecific modification and disruption of proteins, phospholipids and nucleic acids.6) Critical sites of ROS attack are the cell membrane and the membranes of intracellular organelles. The disruptive effects of ROS involve membrane lipid per-oxidation and membrane protein modification, which may produce alterations in the membrane structure and function including fluidity, permeability, enzyme activity, ion channels, transporter and receptor proteins.7) The role of ROS has been implicated in many human degenerative diseases of aging. Various antioxidants have been found to have some preventive and therapeutic effects on these diseases induced by ROS.8) Therefore, substantial efforts have been made in recent years to identify both natural and synthetic antioxidants. Moutan Cortex Radicis (MCR), the root cortex of Paeonia suffruticosa ANDREWS, is a Chinese herbal medicine widely used as an analgesic, antispasmodic, and anti-inflammatory agent. The drug has also long been used in remedies for female diseases. MCR is reported to inhibit oxidative DNA cleavage 9) and to have a scavenging effect on 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals and superoxide anion radicals generated by the xanthine-xanthine oxidase system. 10)The chemical components of MCR are known to be paeonol, paeonoside, paeonolide, paeoniflorin, benzoylpaeoniflorin, oxypaeoniflorin, benzoyl-oxy-paeoniflorin, and apiopaeonoside.PC12 cells have been widely used as an in vitro experimental model to study the effects of various neurotoxic agents, including 6-hydroxydopamine, 1-methyl-4-phenylpyridinium (MPP ϩ ), paraquat, and manganese on dopaminergic cells.11,12) PC12 cells are electrically excitable and neurosecretory (dopamine, norepinephrine, and/or acetylcholine), and contain many membrane-bound and cytosolic macromolecules associated with neurons.11)The present study was designed to investigate whether ethanol extract of MCR is capable of...

Moutan cortex, (MC) is one of the most widely used Oriental herbal medicines for treating inflammatory diseases. In this study, the effect of MC on lipopolysaccharide (LPS) and recombinant interferon‐gamma (rIFN‐γ)‐induced production of nitric oxide (NO) and tumor necrosis factor (TNF)‐alpha were examined using mouse peritoneal macrophages. MC inhibited the LPS/rIFN‐γ‐induced expression of inducible nitric oxide synthase (iNOS) and TNF‐alpha release. To clarify the mechanism involved, the effect of MC on the activation of nuclear factor (NF)‐kappaB was examined. The LPS/rIFN‐γ‐induced activation of NF‐kappaB was almost completely blocked by MC at 0.5 mg/ml. These findings demonstrate that the inhibition of the LPS/rIFN‐γ‐induced production of NO and TNF‐alpha by MC is due to the inhibition of NF‐kappaB activation.