Fibroblast growth factor-2 (FGF-2) regulates several vascular endothelial cell functions, including proliferation. It has been suggested that the regulation may be modulated by reactive sulfur species (RSS), which are hydrogen sulfide and biomolecules containing persulfide/polysulfide groups. Since RSS promote vascular endothelial cell proliferation, we hypothesized that FGF-2 regulates the levels of RSS-producing enzymes in the cells. Bovine aortic endothelial cells were cultured and treated with FGF-2, and intracellular RSS levels were determined. The expression of RSS-producing enzymes, cystathionine γ-lyase (CSE), cystathionine β-synthase, 3-mercaptopyruvate sulfurtransferase, and cysteinyl-tRNA synthetase 2, was evaluated, and the intracellular signaling pathway that mediates FGF-2 regulation of RSS accumulation was investigated. We revealed that FGF-2 upregulates the expression of RSS by selectively inducing CSE via the ERK1/2 signaling pathway in vascular endothelial cells. The effect of FGF-2 on the function of vascular endothelial cells may be modulated by intracellular RSS, especially higher-molecular-mass RSS such as protein persulfide, the levels of which are increased by the growth factor.
In this study, we analyzed the volatile organic compounds (VOCs) emitted from a sample of bedding products. These items are intended for long-term use indoors and therefore will be present for long periods of time in the breathing zone of household occupants. Forty bedding products (20 pillows and 20 mattresses) were obtained from the Japanese domestic market for analysis. We have pioneered the measurement of VOCs from bedding products using the sampling bag method, and our measurements showed that a variety of VOCs were emitted from the items. In the pillow sample, polyethylene pillows emitted the most aliphatic hydrocarbons, while buckwheat hull pillows emitted fewer chemicals overall. All pillows emitted tetradecane, toluene, and xylene. VOCs emissions from the mattresses tended to be higher than from the pillows. The mattresses emitted 2-ethyl-1-hexanoic acid frequently and at high concentrations. To further understand the effects of indoor air pollution, it is necessary to continue research into testing the emissions from bedding products and other household items.
This cross-sectional study examined the sociodemographic characteristics associated with energy drink consumption at a medical and welfare university in Japan. Data were collected and analyzed from 1249 students (first to fourth year) belonging to a single university. We examined 19 sociodemographic variables through a questionnaire. Furthermore, we identified sociodemographic characteristics associated with the consumption of energy drinks using multivariate logistic regression analysis. We characterized students who consumed energy drinks using principal component analysis and hierarchical cluster analysis. Significance was established at P < 0.05. The findings of our study revealed that perceived stress (P = 0.01) and experiencing strong sleepiness (P = 0.01) during the day in males and females, as well as the frequency of alcoholic drink consumption were related to the habitual consumption of energy drinks. The students who consumed energy drinks were categorized into three clusters: male students who perceived stress, female students who perceived stress and wanted to consume alcohol, and male students who perceived stress and experienced excessive daytime sleepiness. Thus, perceived stress may be strongly correlated with the consumption of energy drinks. Therefore, educational interventions to promote awareness of the health risks of excessive energy drink consumption among students are warranted.
Indoxyl sulfate is a uremic toxin and is difficult to remove by hemodialysis owing to its tight binding to albumin in the blood. There is therefore concern that it could cause inflammatory responses in renal tissue, leading to worsening of renal failure. Recent reports suggest that indoxyl sulfate not only directly affects renal cells but also induces an inflammatory response via macrophages infiltrating renal tissues. However, the mechanism of the indoxyl-sulfate-induced inflammatory response mediated by macrophages and the effect of macrophages on renal cells have not yet been elucidated. Here, we evaluated the effect of indoxyl sulfate on the inflammatory response of macrophages and the effect of macrophages on renal cells. Indoxyl sulfate upregulated the expression of tumor necrosis factor-α (TNF-α) by THP-1 macrophages. Moreover, it activated the transcriptional regulator nuclear factor-kappa B (NF-κB) p65, and an inhibitor of NF-κB suppressed indoxyl-sulfate-induced TNF-α elevation. Supernatant of THP-1 macrophages treated with indoxyl sulfate increased the mRNA expression levels of inflammatory cytokines in HK-2 renal proximal tubular epithelial cells. These results suggest that indoxyl sulfate increases TNF-α expression through the activation of NF-κB in THP-1 macrophages and that macrophages stimulated with indoxyl sulfate induce an inflammatory response in the proximal tubular epithelial cells.
We and others have previously reported the possible usefulness of (–)-xanthatin, one of the naturally occurring xanthanolides present in the Cocklebur plant, as an anticancer cytotoxic agent in both in vivo and in vitro settings. Anticancer agents generally act as a double-edged sword during cancer chemoprevention, as these drugs can cause infertility in males and females. Although (–)-xanthatin is known to be an anti-proliferator against cancer cells, the adverse effect on spermatogenesis has not yet been investigated, even in vitro. In this study, we utilized chemically synthesized pure (–)-xanthatin to analyze whether this molecule affects the appearance of haploid cells in the population of a GC-2spd(ts) cell line, an in vitro model of male germ cells. We did not observe any remarkable effects on the haploid formation of GC-2spd(ts) at a (–)-xanthatin concentration below 0.5 μM.
Dementia is expected to affect an increasing number of patients with global aging populations. About 70% of all dementia is related to Alzheimer's disease (AD). Overaccumulation of amyloid-β protein (Aβ) in the brain forms senile plaques, one of the main features of neurodegeneration in AD. However, there are few drugs available to specifically inhibit senile plaque formation. Fucoidan, a sulfated polysaccharide derived from brown algae, has various bioactivities, such as anti-tumoral and anti-obesity effects. This study aimed to clarify the mechanism underlying the protective effect of fucoidan against Aβ-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Cell viability and Aβ-induced cytotoxicity were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, calcein AM, and ethidium homodimer-1. Aβ-induced oxidative stress was evaluated through reactive oxygen species (ROS), cell membrane phospholipid peroxidation, mitochondrial ROS, and Mn-SOD, a mitochondrial radical scavenger. In addition, mitochondrial membrane permeability transition, and ATP concentration were evaluated. Fucoidan significantly improved Aβ-reduced cell viability. With respect to oxidative stress, Aβ exposure increased ROS, lipid peroxidation, and mitochondrial ROS, while fucoidan significantly suppressed these changes. Fucoidan also suppressed the decline in mitochondrial permeability transition and ATP caused by Aβ. Therefore, through its numerous antioxidant activities, fucoidan might have a neuroprotective role in preventing Aβ-induced neurotoxicity.