Ashland showcases skin defence plankton extract in China
U.S. supplier Ashland is using the platform to show the skin defence effects of its GP4G SP biofunctional compound which is designed for use in formulations to better manage the appearance of skin following exposure to solar and thermal shocks.
“Protecting skin from the environmental shocks of infrared and UV radiation, as well as extreme heat and cold may be the most efficient way to defend against the look of premature skin ageing,” says Neil Astles, global marketing manager, skin care biofunctionals, Ashland Specialty Ingredients.
“New clinical research on GP4G SP biofunctional, an offering commercially available from Vincience since 1994, demonstrates how a novel nucleotide found in nature, a building block of DNA and RNA, may be used in various capacities to help preserve skin appearance ex vivo in the presence of otherwise harmful environmental shocks.”
Ashland will present its new data at PCHi demonstrating how plankton extract rich in GP4G nucleotides limits the appearance of skin damage ex vivo following exposure to environmental shocks.
Research conducted at Ashland’s Vincience Global Skin Research Laboratory in southeast France has been focusing on strategies to defend skin with a topical application of guanine rich nucleotides extracted from Artemia salina, a type of plankton proven to withstand extreme environmental conditions over millions of years.
These nucleotides are believed to be a source of free energy during a prolonged absence of oxygen, and have helped the species adopt and survive environmental shocks for millions of years.
Armed with this knowledge, the Vincience research team investigated potential associations between GP4G nucleotides and a reduction in indicators of human skin damage from infrared radiation.
Their work confirmed that when exposed to a certain dose of IR-A, human keratinocytes showed marked increases in reactive oxygen species (ROS) production in vitro.
Coating human keratinocytes with just 1% GP4G SP biofunctional led to a limited increase in production of ROS in vitro for cells exposed to the same level of IR-A.