Environmental contaminants such as dioxins enter the body mainly through diet and cause various toxicities through transformation of the aryl hydrocarbon receptor (AhR). We previously reported that certain natural flavonoids at the dietary level suppress the AhR transformation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In this study, we identified lutein and chlorophyll a and b from green tea leaves as the novel antagonists for AhR. These active compounds suppressed AhR transformation dose-dependently with the 50% inhibitory concentration (IC(50)) values against 0.1 nM TCDD-induced AhR transformation at 3.2, 5.0, and 5.9 microM, respectively. (-)-Epigallocatechin gallate, which is the most abundant flavonoid in green tea leaves, also showed stronger suppressive effects than did other major tea components, with the IC(50) value of 1.7 microM. Thus, these pigments of green tea leaves have the potential to protect from dioxin toxicity through the suppression of AhR transformation.
This study aimed to investigate the influence of carbonated drinks with gas volumes (GV) of 0, 1.5, and 2.7 on linguapalatal swallowing pressure, intraoral carbonation perception, and maximum velocity of a bolus through the pharynx in healthy volunteers (N = 20, all female, age range; 20-21 years). The volunteers swallowed a 12-mL drink in the natural state. Linguapalatal swallowing pressure was measured using a special sensor sheet, and maximum velocity of the bolus through the pharynx was measured using ultrasonic diagnostic imaging equipment. Peak magnitude, integrated value, and duration of linguapalatal swallowing pressure and maximum velocity of a liquid bolus through the pharynx increased with an increase in carbon dioxide content in the carbonated drink. The total integrated values of carbonated drinks with GV of 1.5 and 2.7 were larger than that of the drink without carbon dioxide. These results suggest that the carbon dioxide dissolved in carbonated drinks influences the activity of taste receptors in the mouth and results in neuromotor responses.
Botulinum neurotoxin type A (BoNT/A, 1.5 nM) completely inhibited indirectly evoked twitches in in vitro mouse phrenic nerve-diaphragm preparations within 40 ± 45 min. Black tea extract, thearubigin fraction (TRB), mixed with BoNT/A blocked the inhibitory eect of the toxin. The protective eect of TRB extended to botulinum neurotoxins types B and E (BoNT/B and BoNT/E) and tetanus toxin, but not to tetrodotoxin. TRB was also eective against oral toxicity of BoNT/A, B and E. Thus, TRB may be of potential bene®t in protecting the paralytic actions of botulinum neurotoxins (BoNTs), but its use is limited by mixing with the toxin.
Abstract:The aim of the present study was to elucidate the mechanism of the protective effect of black tea extract, the thearubigin fraction, against the neuromuscular blocking action of botulinum neurotoxin types A, B, and E. The effects of thearubigin fraction extracted from a black tea infusion were examined on the neuromuscular blocking action of botulinum neurotoxin types A, B, and E in mouse phrenic nerve-diaphragm preparations and on the binding of these toxins to rat cerebrocortical synaptosomes. Botulinum neurotoxin type A (1.5 nM), B (6 nM), or E (5 nM) abolished indirect twitches in mouse phrenic nerve-diaphragm preparations within 50, 90, 90 min., respectively. Thearubigin fraction mixed with each toxin blocked the inhibitory effect of the toxins. The specific binding of [ 125 I]botulinum neurotoxin type A, B, or E to rat cerebrocortical synaptosomes was inhibited by mixing iodinated toxin with thearubigin fraction. The elution profile of [ 125 I]botulinum neurotoxin type A, B, or E on Sephadex G-50 column chromatography was different from that of toxin mixed with thearubigin fraction. These findings indicate that thearubigin fraction protects against the neuromuscular blocking action of botulinum neurotoxin types A, B, and E by binding with the toxins.
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