Nation-Based Occurrence and Endogenous Biological Reduction of Mycotoxins in Medicinal Herbs and Spices.

Medicinal herbs have been increasingly used for therapeutic purposes against a diverse range of human diseases worldwide. Moreover, the health benefits of spices have been extensively recognized in recent studies. However, inevitable contaminants, including mycotoxins, in medicinal herbs and spices can cause serious problems for humans in spite of their health benefits. Along with the different nation-based occurrences of mycotoxins, the ultimate exposure and toxicities can be diversely influenced by the endogenous food components in different commodities of the medicinal herbs and spices. The phytochemicals in these food stuffs can influence mold growth, mycotoxin production and biological action of the mycotoxins in exposed crops, as well as in animal and human bodies. The present review focuses on the occurrence of mycotoxins in medicinal herbs and spices and the biological interaction between mold, mycotoxin and herbal components. These networks will provide insights into the methods of mycotoxin reduction and toxicological risk assessment of mycotoxin-contaminated medicinal food components in the environment and biological organisms.

Effects of seaweed Laminaria japonica extracts on skin moisturizing activity in vivo.

Twelve species of edible seaweed from the coast of Korea were screened for skin moisturizing activity. We placed the lead of a Corneometer on an approximately 6-cm2 test area of the forearm and measured both untreated skin (control) and skin treated with test moisturizing creams either containing or not containing 5% water:propylene glycol (50:50) extracts of seaweeds. Over the 8-h observation period, the strongest activity of the Laminaria japonica extracts occurred at the 2-h period. For the 10% extract, hydration with the L. japonica extract increased by 14.44% compared with a placebo. Transepidermal water loss (TEWL) was also measured using a test cream with 10% L. japonica extract. For up to 8 h after applying the creams, TEWL was decreased to 4.01 g/cm2, which was approximately 20% of that seen with the control. We suggest that the L. japonica extract hydrates skin via the humectants and hydrocolloids that it contains. To confirm the safety of L. japonica extracts, we performed a patch test on human skin. The results suggested that at moderate doses humans can safely use the extracts. For commercial applications, we evaluated the physicochemical characteristics of the test cream products, including Hunter L, a, and b values; pH; refractive index; and coefficient of viscosity. L. japonica extract did not affect overall formulations of the test cream product in any of the tested aspects. These results suggest that L. japonica extract is a promising ingredient in moisturizing formulations.

Pinoresinol-4,4'-di-O-beta-D-glucoside from Valeriana officinalis root stimulates calcium mobilization and chemotactic migration of mouse embryo fibroblasts.

Lignans are major constituents of plant extracts and have important pharmacological effects on mammalian cells. Here we showed that pinoresinol-4,4'-di-O-beta-D-glucoside (PDG) from Valeriana officinalis induced calcium mobilization and cell migration through the activation of lysophosphatidic acid (LPA) receptor subtypes. Stimulation of mouse embryo fibroblast (MEF) cells with 10 microM PDG resulted in strong stimulation of MEF cell migration and the EC(50) was about 2 microM. Pretreatment with pertussis toxin (PTX), an inhibitor of G(i) protein, completely blocked PDG-induced cell migration demonstrating that PDG evokes MEF cell migration through the activation of the G(i)-coupled receptor. Furthermore, pretreatment of MEF cells with Ki16425 (10 microM), which is a selective antagonist for LPA(1) and LPA(3) receptors, completely blocked PDG-induced cell migration. Likewise, PDG strongly induced calcium mobilization, which was also blocked by Ki16425 in a dose-dependent manner. Prior occupation of the LPA receptor with LPA itself completely blocked PDG-induced calcium mobilization. Finally, PDG-induced MEF cell migration was attenuated by pretreatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor such as LY294002. Cells lacking downstream mediator of PI3K such as Akt1 and Akt2 (DKO cells) showed loss of PDG-induced migration. Re-expression of Akt1 (but not Akt2) completely restored PDG-induced DKO cell migration. Given these results, we conclude that PDG is a strong inducer of cell migration. We suggest that the pharmacological action of PDG may occur through the activation of an LPA receptor whereby activation of PI3K/Akt signaling pathway mediates PDG-induced MEF cell migration.