ANTI-POLLUTION
Mitochondrial protection and apoptosis prevention Excessive ROS accumulation damages mitochondria, leading to dysfunction and apoptosis. Mitochondrial membrane potential is a key indicator of mitochondrial health, and changes in this potential occur in the early stages of apoptosis. We assessed these changes using JC-1
fluorescent staining, where the red-to-green fluorescence ratio indicates membrane potential. Blue light exposure significantly reduced this ratio, suggesting mitochondrial depolarization and increased apoptosis. Tocotrienol treatment restored the ratio, whereas this effect was not observed in the alpha-tocopherol group (Figure 2). Further analysis revealed that blue light
exposure activated the p38-MAPK apoptotic pathway, increasing phosphorylated p38 and cleaved caspase-3 levels. Alpha-tocopherol reduced phosphorylated p38 but had no effect on cleaved caspase-3, whereas DavosLife E3 Tocotrienols significantly reduced both markers. This suggests that tocotrienols protect
cells from mitochondria-mediated apoptosis by reducing phosphorylated p38 and cleaved caspase-3 levels, thereby preserving mitochondrial membrane potential.6
Regulation of hyperpigmentation We examined the role of DavosLife E3 Tocotrienols in regulating tyrosinase activity and melanin synthesis. Blue light exposure significantly increased intracellular and extracellular melanin levels. Tocotrienol treatment reduced both parameters, demonstrating a protective effect against hyperpigmentation. Additionally, tyrosinase activity was
significantly lowered with tocotrienol treatment compared to alpha-tocopherol, reinforcing their role in pigmentation regulation.
A natural shield against air pollution Beyond blue light, another major contributor to oxidative stress is airborne pollution. The skin acts as a barrier against environmental stressors, but pollutants such as particulate matter (PM2.5) can penetrate the skin via hair follicles or the stratum corneum, inducing
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www.personalcaremagazine.com Tocopherol Alpha-
DavosLife E3 Tocotrienols
Blue light (38J/cm2 +
‒ ) ‒ +
Alpha-Tocopherol (20µM)
DavosLife E3 Tocotrienols (20µM)
Figure 3: Intracellular and extracellular melanin levels of cells induced by blue light (BL) and treatment April 2025 PERSONAL CARE
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oxidative stress and weakening the skin barrier. This can lead to tissue and DNA damage,
protein carbonylation, and lipid peroxidation, reducing keratinocyte viability. An impaired skin barrier allows deeper penetration of pollutants, which activates matrix metalloproteinases (MMPs), accelerating extracellular matrix degradation and skin ageing.7 To evaluate the protective effects of
DavosLife E3 Tocotrienols against PM2.5 exposure, we assessed ROS levels in HaCaT cells. PM2.5 exposure increased intracellular ROS levels approximately 2.5-fold compared to the sham group. At an equal concentration (20 µM),
DavosLife E3 Tocotrienols demonstrated greater efficacy than alpha-tocopherol in reducing ROS generation after exposure to 100 µg/mL PM2.5. These findings suggest that DavosLife E3 Tocotrienols inhibit PM2.5-induced cytotoxicity by suppressing excessive ROS production (Figure 5).
Suppression of PM2.5-induced MAPK and COX-2 activation The MAPK pathway is involved in PM2.5-induced inflammation, apoptosis, and skin barrier function modulation.8
Our study showed that
DavosLife E3 Tocotrienols suppressed PM2.5- induced MAPK and COX-2 activation. Western
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Tocopherol Alpha-
DavosLife E3 Tocotrienols
Blue light (38J/cm2 +
‒ ) ‒ + Tocopherol Alpha- Blue light (38J/cm2 + ‒ ) ‒ +
Figure 2: Quantification of red/green fluorescence ratio to represent the polarization of the membrane potential. Data shown are expressed as % of sham and expressed as mean ± SEM
blot analysis confirmed that 100 µg/mL PM2.5 activated p38, JNK1/2, and ERK phosphorylation in HaCaT cells. Treatment with 20 µM DavosLife E3
Tocotrienols significantly downregulated phosphorylation of these proteins by 61%, 70%, and 24%, respectively. In contrast, alpha- tocopherol did not strongly inhibit MAPK phosphorylation.8 COX-2 expression levels were also evaluated
to examine the downstream effects of MAPK activation. PM2.5 exposure increased COX- 2 protein expression, whereas DavosLife E3 Tocotrienols strongly inhibited COX-2 expression, showing greater efficacy than alpha-tocopherol (Figure 6). Skin barrier integrity relies on key structural
proteins. Filaggrin (FLG) is essential for skin barrier development and hydration. Transglutaminase-1 (TGM-1) facilitates protein cross-linking, strengthening the barrier, while involucrin (IVL) provides structural support. PM2.5 exposure significantly reduced the expression of these proteins, compromising skin barrier function. Treatment with DavosLife E3 Tocotrienols
restored FLG, TGM-1, and IVL levels by 50%, 20%, and 68%, respectively (Figure 7), whereas alpha- tocopherol did not significantly restore these proteins. This highlights the superior efficacy of
DavosLife E3 Tocotrienols
49
% Intracellular Melanin Levels (
W.r.t.sham)
Red: Green Ratio (% Control)
% Extracellular Melanin Levels (
W.r.t.sham)
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