Six-month low level chlorine dioxide gas inhalation toxicity study with two-week recovery period in rats

<p>Abstract</p> <p>Background</p> <p>Chlorine dioxide (CD) gas has a potent antimicrobial activity at extremely low concentration and may serve as a new tool for infection control occupationally as well as publicly. However, it remains unknown whether the chronic exposure of CD gas concentration effective against microbes is safe. Therefore, long-term, low concentration CD gas inhalation toxicity was studied in rats as a six-month continuous whole-body exposure followed by a two-week recovery period, so as to prove that the CD gas exposed up to 0.1 ppm (volume ratio) is judged as safe on the basis of a battery of toxicological examinations.</p> <p>Methods</p> <p>CD gas at 0.05 ppm or 0.1 ppm for 24 hours/day and 7 days/week was exposed to rats for 6 months under an unrestrained condition with free access to chow and water in a chamber so as to simulate the ordinary lifestyle in human. The control animals were exposed to air only. During the study period, the body weight as well as the food and water consumptions were recorded. After the 6-month exposure and the 2-week recovery period, animals were sacrificed and a battery of toxicological examinations, including biochemistry, hematology, necropsy, organ weights and histopathology, were performed.</p> <p>Results</p> <p>Well regulated levels of CD gas were exposed throughout the chamber over the entire study period. No CD gas-related toxicity sign was observed during the whole study period. No significant difference was observed in body weight gain, food and water consumptions, and relative organ weight. In biochemistry and hematology examinations, changes did not appear to be related to CD gas toxicity. In necropsy and histopathology, no CD gas-related toxicity was observed even in expected target respiratory organs.</p> <p>Conclusions</p> <p>CD gas up to 0.1 ppm, exceeding the level effective against microbes, exposed to whole body in rats continuously for six months was not toxic, under a condition simulating the conventional lifestyle in human.</p

The Response of Blood Pressure of Men at Work to Humid Heat

The present paper described the response of blood pressure of men at work to humid heat for the purpose of determining the permissible limit of environmental heat. From the practical viewpoint of industrial health, the upper permissible limit of humid heat seemed to be 30°-31°C wet bulb temperature and yet around 90°F effective temperature

The Response of Blood Pressure in the Sitting Position to Humid Heat

The experimental study was designed to elucidate the response of blood pressure in the sitting position to humid heat for the purpose of determining the permissible limit of environmental heat. The upper permissible limit of humid heat seemed to be around 33°C wet bulb and yet around 95°F effective temperature

The Response of Blood Pressure to Humid Heat

The experimental study was conducted to throw light on the response of blood pressure of men to humid heat and to determine the permissible limits of environmental heat. The physiological disequilibrium seemed to be imminent sooner or later in the exposure to the humid heat of 95° F effective temperature (33-34°C wet bulb temperature) or more. Therefore, the permissible upper limits of environmental heat seemed to be around 95°F effective temperature

Contribution of renal angiotensin II type I receptor to gene expressions in hypertension-induced renal injury

Contribution of renal angiotensin II type I receptor to gene expressions in hypertension-induced renal injury. Recent evidence indicates that transforming growth factor-β1 (TGF-β1) plays an important role in renal fibrosis via stimulation of extracellular matrix synthesis. The present study was undertaken to investigate the role of angiotensin II type I receptor (AT1 receptor) in hypertension-induced renal injury. Twenty-two-week-old stroke-prone spontaneously hypertensive rats (SHRSP), which had established hypertension and moderate renal damage, were orally given TCV-116, a selective non-peptide AT1 receptor antagonist (0.1, 1 or 10 mg/kg/day), enalapril (10 mg/kg/day) or vehicle once a day for 10 weeks. At the end point of the treatment, we examined renal function, the gene expressions of TGF-β1 and extracellular matrix components in the interstitium [collagen types I (COI) and III (COIII), fibronectin (FN)] and the basement membrane (COIV and laminin), and renal microscopic morphology in rats aged 32 weeks. In vehicle-treated 32 week-old SHRSP with renal dysfunction and nephrosclerosis, renal mRNA levels for TGF-β1, COI, COIII, FN, COIV were all several-fold higher than in WKY. Thus, renal TGF-β1 gene expression was enhanced in SHRSP, which may contribute to the increased renal expressions of COI, COIII, FN, COIV in SHRSP. Treatment with TCV-116 (0.1 mg/kg/day) in SHRSP, in spite of no reduction of blood pressure, decreased renal mRNA levels for TGF-β1, COI, COIII, FN, COIV, being accompanied by the significant decrease in urinary protein and albumin excretion, blood urea nitrogen and plasma creatinine. Treatment with TCV-116 (10 mg/kg/day) in SHRSP decreased mRNAs for TGF-β1, COI, COIII, FN and COIV to almost the same levels as WKY, being associated with normalization of urinary protein and albumin excretion and the prevention of nephrosclerosis, as judged by microscopic histological observations. On the other hand, the effects of enalapril (10 mg/kg/day) on the above mentioned mRNA levels, renal function and renal morphology were weaker than those of TCV-116 (10 mg/kg/day) and were as much as TCV-116 (1 mg/kg/day). These results suggest that independently of hypotensive action, AT1 receptor antagonist has a potent renal protective effect by inhibiting the gene expression of renal TGF-β1 and extracellular matrix components

近年の狭山丘陵における中型哺乳類の生息状況とその変化-アライグマの定着・増加による在来哺乳類への影響-

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