Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice.

BACKGROUND/AIM: Silibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lung injury. MATERIALS AND METHODS: Eight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1ß) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts. RESULTS: Silibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils. CONCLUSION: These findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants.

Monitoring, exposure and risk assessment of formaldehyde in alcoholic beverages in Korea.

Formaldehyde occurs naturally in food and alcoholic beverages. Formaldehyde and alcoholic beverages can cause various health problems, including irritation of the eyes, nose, and throat, respiratory problems, and skin rashes. Alcoholic beverage samples (N = 236) were collected and analyzed for formaldehyde by liquid chromatography-tandem mass spectrometry. The highest average concentrations were detected in fruit wines (1.71 µg/g), followed by wines (1.15 µg/g), cheongju (0.95 µg/g), soju (0.85 µg/g), takju (0.64 µg/g) and beers (0.61 µg/g). We assessed the exposure and risk assessment to formaldehyde from alcoholic beverages based on the monitoring data for the general population and consumers in Korea using various schemes for point estimation. The daily intakes of formaldehyde for the general population and consumers were estimated to be 83 µg and 1202 µg, respectively. The mean hazard indexes (HI) for the general population and consumers in Korea were 0.009 and 0.132, respectively. On the other hand, the mean hazard indexes (HI) for the general population and consumers in Korea were 0.009 and 0.132, respectively. The exposure to formaldehyde in these alcoholic beverages for the Korean population was shown to be of low concern, but it is necessary to monitor the level of formaldehyde in alcoholic beverages and continuously conduct exposure assessment for consumers.

Ginger-derived compounds exert in vivo and in vitro anti-asthmatic effects by inhibiting the T-helper 2 cell-mediated allergic response.

6-Shogaol (SHO) and 6-gingerol (GIN), naturally derived compounds of ginger (Zingiber officinale Roscoe), have been found to have anti-allergic effects on dermatitis-like skin lesions and rhinitis. Although SHO and GIN have demonstrated a potential in various inflammatory diseases, their efficacy and mechanism in asthma have not been largely examined. Therefore, the present study demonstrated the anti-asthmatic effects of SHO and GIN on the T-helper (Th) 2 cell-mediated allergic response pathway in an ovalbumin (OVA)-induced asthma mouse model. The asthma mouse model was established with an intraperitoneal (i.p.) injection of 50 µg OVA and 1 mg aluminum hydroxide with or without an i.p. injection of SHO and GIN (10 mg/kg) before treatment with OVA. In addition, the current study assessed mast cell degranulation in antigen-stimulated RBL-2H3 cells under different treatment conditions (SHO or GIN at 0, 10, 25, 50 and 100 nM) and determined the mRNA and protein levels of anti-oxidative enzymes [superoxide dismutase (SOD)1, SOD2, glutathione peroxidase-1/2, catalase] in lung tissues. SHO and GIN inhibited eosinophilia in the bronchoalveolar lavage fluids and H&E-stained lung tissues. Both factors also decreased mucus production in periodic acid-Schiff-stained lung tissues and the levels of Th2 cytokines in these tissues. GIN attenuated oxidative stress by upregulating the expression levels of anti-oxidative proteins. In an in vitro experiment, the degranulation of RBL-2H3 rat mast cells was significantly decreased. It was found that SHO and GIN effectively suppressed the allergic response in the mouse model by inhibiting eosinophilia and Th2 cytokine production. Collectively, it was suggested that SHO can inhibit lung inflammation by attenuating the Th2 cell-mediated allergic response signals, and that GIN can inhibit lung inflammation and epithelial cell remodeling by repressing oxidative stress. Therefore, SHO and GIN could be used therapeutically for allergic and eosinophilic asthma.

Inhalation of ammonium sulfate and ammonium nitrate adversely affect sperm function.

Among the components of air pollution in developing countries and Asia, (NH4)2SO4 and NH4NO3 are known as major water-soluble in-organic compounds that cause particulate matter. Several researchers have been reported that the (NH4)2SO4 and NH4NO3 induce abnormal decreases in body weight, as well as pneumotoxic, and immunotoxic. Moreover, while it has been reported that (NH4)2SO4 and NH4NO3 have detrimental effects on reproduction, specific effects on male fertility have not been addressed in depth. Therefore, the present study evaluated the reproductive toxicity of (NH4)2SO4 and NH4NO3 in spermatozoa under the capacitation condition. Results showed that various sperm motion parameters were significantly altered after inhalation of (NH4)2SO4 and NH4NO3. In particular, alterations to a range of motion kinematic parameters and to capacitation status were observed after capacitation. In addition, protein kinase A (PKA) activity and tyrosine phosphorylation were altered by (NH4)2SO4 and NH4NO3 regardless of capacitation. Taken together, our results show that inhalation of (NH4)2SO4 and NH4NO3 may induce adverse effects on male fertility such as sperm motility, motion kinematics, and capacitation status via unusual tyrosine phosphorylation by abnormal PKA activity. Therefore, we suggest that exposure to (NH4)2SO4 and NH4NO3 should be highlighted as a health risk, as it may lead to male reproductive toxicity in humans and animals.

Vanadium adversely affects sperm motility and capacitation status via protein kinase A activity and tyrosine phosphorylation.

Vanadium is a chemical element that enters the atmosphere via anthropogenic pollution. Exposure to vanadium affects cancer development and can result in toxic effects. Multiple studies have focused on vanadium's detrimental effect on male reproduction using conventional sperm analysis techniques. This study focused on vanadium's effect on spermatozoa following capacitation at the molecular level, in order to provide a more detailed assessment of vanadium's reproductive toxicity. We observed a decrease in germ cell density and a structural collapse of the testicular organ in seminiferous tubules during vanadium treatment. In addition, various sperm motion parameters were significantly decreased regardless of capacitation status, including sperm motility, rapid sperm motility, and progressive sperm motility. Curvilinear velocity, straight-line velocity, average path velocity, beat cross frequency, and mean amplitude of head lateral displacement were also decreased after capacitation. Capacitation status was altered after capacitation. Vanadium dramatically enhanced protein kinase A (PKA) activity and tyrosine phosphorylation. Taken together, our results suggest that vanadium is detrimental to male fertility by negatively influencing sperm motility, motion kinematics, and capacitation status via abnormal PKA activity and tyrosine phosphorylation before and after capacitation.