Factor analysis approach unveils the influencing factors of dandruff in the normal teenage population.

The aim of this study was to explore the main factors affecting the occurrence of dandruff in healthy people (nondisease-induced scalp desquamation). This study analyzed the fungal microbial diversity of the scalp in Chinese teenage volunteers and measured scalp sebum secretion, the scalp pH value, and scalp transepidermal water loss. The amount and size of dandruff were measured, and the main factors that influence dandruff in the normal population were identified using principal component analysis. The results showed that an increase in Malassezia restricta led to an increased amount of dandruff in the mild and moderate groups. Conversely, this was not found for individuals in the severe group, whose dandruff symptoms were influenced by scalp barrier function. In terms of dandruff area grouping, the pH value and the amount of sebum secretion were the main factors, with the barrier function and microbial diversity being secondary factors. Dandruff cosmetics should emphasize different treatments for different types of dandruff to achieve better antidandruff effects. The results of this study provide a new theoretical basis for the development of multiple targets for antidandruff agents aimed at the normal population.

Protective effect of oat bran extracts on human dermal fibroblast injury induced by hydrogen peroxide.

Oat contains different components that possess antioxidant properties; no study to date has addressed the antioxidant effect of the extract of oat bran on the cellular level. Therefore, the present study focuses on the investigation of the protective effect of oat bran extract by enzymatic hydrolysates on human dermal fibroblast injury induced by hydrogen peroxide (H(2)O(2)). Kjeldahl determination, phenol-sulfuric acid method, and high-performance liquid chromatography (HPLC) analysis indicated that the enzymatic products of oat bran contain a protein amount of 71.93%, of which 97.43% are peptides with a molecular range from 438.56 to 1301.01 Da. Assays for 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity indicate that oat peptide-rich extract has a direct and concentration-dependent antioxidant activity. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) colorimetric assay and the TdT-mediated digoxigenin-dUTP nick-end labeling (TUNEL) assay for apoptosis showed that administration of H(2)O(2) in human dermal fibroblasts caused cell damage and apoptosis. Pre-incubation of human dermal fibroblasts with the Oatp for 24 h markedly inhibited human dermal fibroblast injury induced by H(2)O(2), but application oat peptides with H(2)O(2) at same time did not. Pre-treatment of human dermal fibroblasts with Oatp significantly reversed the H(2)O(2)-induced decrease of superoxide dismutase (SOD) and the inhibition of malondialdehyde (MDA). The results demonstrate that oat peptides possess antioxidant activity and are effective against H(2)O(2)-induced human dermal fibroblast injury by the enhanced activity of SOD and decrease in MDA level. Our results suggest that oat bran will have the potential to be further explored as an antioxidant functional food in the prevention of aging-related skin injury.

Hydrogen peroxide enhanced Ca(2+)-activated BK currents and promoted cell injury in human dermal fibroblasts.

AIMS: Recent studies have shown that dermal fibroblasts possess multiple types of voltage-dependent K(+) channels, and the activation of these channels induces apoptosis. In the present study, we aimed to investigate whether hydrogen peroxide (H(2)O(2)), an oxidative stress inducer, could modulate these channels or induce human dermal fibroblasts injury. MAIN METHODS: The effects of H(2)O(2) on K(+) currents were studied using a whole-cell recording. Intracellular PKC levels were measured with a direct human PKC enzyme immunoassay kit. Cell viability was assessed using PI staining and apoptotic nuclei were detected with TdT-mediated digoxigenin-dUTP nick-end labelling assay (TUNEL) assay. KEY FINDINGS: Treatment of cells with 100µM H(2)O(2) resulted in a partially reversible increase in non-inactivating outward K(+) currents and an alteration in the steady-state activation property of the channels. The H(2)O(2)-induced increase in K(+) currents was mimicked by a PKC activator, and was blocked by the PKC inhibitor or the large conductance Ca(2+)-activited K(+) (BK) channel blockers. The intracellular PKC levels were significantly enhanced by H(2)O(2) treatment in a concentration-dependent manner. After exposure to H(2)O(2), evaluation of fibroblasts survival rate and damaged cell number with TUNEL-positive nuclei revealed an increased cell injury. Blocking the K(+) channels with blockers significantly decreased the H(2)O(2)-induced human dermal fibroblasts injury. SIGNIFICANCE: Our results revealed that H(2)O(2) could enhance BK currents by PKC pathway. Increased K(+) currents might be related to H(2)O(2)-induced human dermal fibroblasts injury. The results reported here contribute to our understanding of the mechanism underlying H(2)O(2)-induced human dermal fibroblasts injury.

ET-1 inhibits B-16 murine melanoma cell migration by decreasing K(+) currents.

Cell migration is mediated by ion channels and transporters, and plays crucial roles in a variety of physiological and pathological processes. Previously, our studies have shown that a Ca(2+)-regulated K(+) current exists in B-16 murine melanoma cells, and that endothelin-1 (ET-1) inhibits the K(+) current via a PKC-dependent pathway. In the present study, patch-clamp whole-cell recording and transwell migration assays were used to examine the effects of ET-1 on B-16 murine melanoma cell migration. ET-1 (100 nM in the injection pipette and 10 nM in the incubation medium) decreased the K(+) current amplitude by 33.0 +/- 2.5% and inhibited migration of B-16 cells by 57.4 +/- 9.4%. Similarly, the Ca(2+)-regulated K(+) channel blockers, BaCl(2) and quinidine, decreased the K(+) current by 20.5 +/- 1.0% and 36.6 +/- 1.2%, respectively, and slowed migration of B-16 melanoma cells by 37.1 +/- 8.6% and 42.7 +/- 8.8%, respectively. The effect of ET-1 on the K(+) current and cell migration was simulated by ET-3. In contrast, the K(+) channel opener, diclofenac, increased the K(+) current by 128.8 +/- 11.7%, 257.4 +/- 35.8% at concentrations of 1 and 5 mM, respectively. Likewise, the migration of B-16 murine melanoma cells dramatically increased by 75.6 +/- 12.7% in the presence of 100 microM diclofenac in incubation medium. Furthermore, the ET-1- and ET-3-induced inhibition of K(+) current and migration was abrogated by diclofenac. In the presence of diclofenac, ET-1 only reduced the K(+) current amplitude by 10.6 +/- 1.1%, and slowed B-16 cell migration by only 10.8 +/- 8.9%. The results suggest that the K(+) channel-dependent migration of B-16 melanoma cells is modulated by ET-1. Cell Motil.

Ca(2+)-inactivated K+ current is modulated by endothelin-1 in B-16 murine melanoma cells.

It is well established that endothelin-1 (ET-1) plays a role in differentiation and proliferation in a variety of cells such as fibroblasts and human melanoma cells via a receptor-mediated mechanism. However, whether ET-1 modulates ion channel activity in these cell types is still unknown. In this report, we recorded the voltage-dependent outward K+ current in cultured B16 melanoma cells using the patch-clamp technique. Biophysical and pharmacological properties of the K+ current, and the effect of ET-1 on the K+ current were investigated. When cells were loaded with a Ca(2+)-chelating agent (EGTA or BAPTA), the K+ current amplitude gradually increased with time after establishment of the whole cell configuration. Replacement of Ca2+ with Co2+ in the extracellular medium caused no significant modulation of the K+ current amplitude. Addition of BaCl2 or quinidine to the extracellular solution reduced the K+ current amplitude, whereas the K+ current was insensitive to tetraethylammonium. ET-1 (10 nM) reversibly decreased the K+ current amplitude and accelerated the decay of the K+ current. The ET-1-induced inhibitory effect displayed no desensitization following repeated ET-1 application. Pretreatment with pertussis toxin (PTX) or perfusion of cells with the protein kinase C (PKC) inhibitor H-7 abolished the inhibitory effect of ET-1 on the K+ current. We conclude that the outward K+ current recorded in murine B-16 melanoma cells represents a Ca(2+)-inactivated K+ current, and that the inhibitory effect of ET-1 on the K+ current may reveal a novel mechanism to control the differentiation and proliferation of melanoma cells.

[Study on mitochondrial DNA damage in peripheral blood nucleate cells of the workers exposed to acrylonitrile].

OBJECTIVE: To study the potential aging effect on workers exposed to acrylonitrile (ACN). METHODS: The deletion rates of mitochondrial DNA (mtDNA) in peripheral blood nucleate cells of 47 exposed workers and 47 non-exposed workers (as control), as well as 12 old people and 12 young people were measured with polymerase chain reaction (PCR). RESULTS: The positive rates of mtDNA deletion in peripheral blood nucleate cells were 17.02% in the workers exposed to ACN and 25.00% in group of old people. However, the mtDNA deletion was not detected in the control group and young people. CONCLUSIONS: ACN could induce mtDNA deletion in peripheral blood nucleate cells of the exposed workers. There may be a potential molecular effect of occupational ACN exposure on workers' aging.