We examined the relationship between the carbonizing temperature of bamboo carbide made from Moso bamboo (Phyllostachys pubescens) and the removal effect of harmful gases and odorants, and the use of a bamboo charcoal as a countermeasure for “Sick Building Syndrome” or “Chemical Sensitivity” and the use as a deodorant. With regard to the carbonizing temperature of the bamboo charcoal, a temperature sensor was installed inside each bamboo material and the carbonizing temperature was controlled at 500, 700 and 1000°C. The removal effect was tested for formaldehyde, toluene and benzene that are known to cause “Sick Building Syndrome” or “Chemical Sensitivity” and for ammonia, indole, skatole and nonenal as odorants. The formaldehyde removal effect was only slightly different in the charcoal at all the carbonizing temperatures. The benzene, toluene, indole, skatole and nonenal removal effect were the highest for the bamboo charcoal carbonized at 1000°C and tended to increase as the carbonizing temperature of the bamboo charcoal increased. The removal effect for ammonia was the highest on the bamboo charcoal carbonized at 500°C. It is concluded that the effective carbonizing temperature is different for each chemical, and a charcoal must be specifically selected for use as an adsorbent or deodorant.
To clarify indoor air pollution, indoor and outdoor air samples were collected from 22 houses in Tokyo using a low-volume cascade impactor with a quartz fiber filter. Suspended particulate matter (SPM) was classified into three sizes: ≥ 10 μm, 2.5-10 μm and ≤ 2.5 μm. The mutagenic compounds were extracted by the dichloromethane/sonication method. The solution was concentrated by N2 gas. Mutagenicity was determined by the microsuspension method, employing the Salmonella typhimurium (S. typhimurium) YG 1024 strain in the presence and absence of S9 mix. The samples showed generally higher mutagenicity in the absence of S9 mix than in its presence. Outdoor air tended to have higher or similar mutagenicity to indoor air. The smallest SPM (≤ 2.5 μm) fraction showed the highest mutagenicity (revertants/m3·air). These results suggest that one of the main sources of high mutagenic SPM indoors is air entering from outdoors.
Acetyl transfer and N-deacetylation associated with the metabolism of carcinogenic 2,4-diaminotoluene (2,4-DAT) were examined by detecting the products formed during the incubation of 2,4-DAT and its known urinary metabolites with the liver cytosol fraction from male Wistar rats. Data obtained from the incubation of 4-acetylamino-2-aminotoluene (4AA2AT) with the liver cytosol in the presence of 2,4-diaminobenzoic acid (2,4-DABA) indicated that the cytosol catalyzes the acetyl transfer between 4AA2AT and 2,4-DABA to produce 2,4-DAT and 2-acetylamino-4-aminobenzoic acid (2AA4ABA). The cytosol also catalyzed the acetyl transfer between 2,4-diacetylaminotoluene (2,4-DAAT) and 2,4-DABA to produce 2-acetylamino-4-aminotoluene (2AA4AT) and 2AA4ABA. Without 2,4-DABA, the cytosol catalyzed the N-deacetylations of 4AA2AT and 2,4-DAAT to produce 2,4-DAT and 2AA4AT. 2AA4AT was inactive for both the N-deacetylation and the acetyl transfer. 2,4-DAT itself was N-acetylated to 4AA2AT by incubation with acetyl-CoA, but 2AA4AT and 2,4-DAAT were not detectable in the incubation product. However, both 2AA4AT and 4AA2AT were N-acetylated to 2,4-DAAT by incubation with acetyl-CoA. These findings suggest that 2,4-DAT is reproduced either by the N-deacetylation of 4AA2AT or by the acetyl transfer between 4AA2AT and 2,4-DABA in the metabolism of 2,4-DAT and further suggest that 2,4-DAAT is produced by the acetyl-CoA-dependent N-acetylation of 4AA2AT; 2AA4AT is produced either by the N-deacetylation of 2,4-DAAT or by the acetyl transfer between 2,4-DAAT and 2,4-DABA. Based on these results, the metabolic pathway of 2,4-DAT in the rat is proposed.
Plasticizers in Japanese retail foods were determined by gas chromatography/mass spectrometry (GC/MS) (SIM). The plasticizers tested were as follows: dibutyl phthalate, butylbenzyl phthalate, di(2-ethylhexyl) phthalate (DEHP), diisononyl phthalate, di(2-ethylhexyl) adipate, diisononyl adipate (DINA), dialkyl adipate, dibutyl sebacate, O-acetyl tributyl citrate (ATBC) and diacetyllauroyl glycerol (DALG). A total of 93samples were analyzed. For the analysis, each sample was extracted by a method suitable to its nature and cleaned using Florisil® and Bondesil PSA® dual layer columns. The recovery of plasticizers from fortified food samples was 62.0-131.0%, except in the case of DINA. The limit of detection (LOD) was different for each sample species and plasticizers. For example, the LOD for plasticizers in retort-pouched baby food was 0.0004-0.037 μg/g. A retort-pouched baby food sample was found to be contaminated by DEHP at the Japanese tolerable daily intake (TDI) level, 40 μgkg/day. The source of contamination was presumed to be disposable gloves because the baby food was produced before the prohibition of DEHP-containing poly vinyl chloride (PVC) gloves by the Japanese government. After that prohibition, products generally contained much lower levels of DEHP. A higher level of DALG was detected in the other baby food samples, although it became clear that DALG did not originate as contamination from plastics but was added as a food additive. ATBC was detected in bottled sake samples at levels of around 3-7 μg/g, having migrated from the gasket of the bottle cap. ATBC and DALG levels in the above foods were quite low compared with their no observed adverse effect level (NOAEL) or guideline levels as food additives.
To examine whether testicular toxicity in rats is caused by a direct effect of mono-butyl phthalate (MBP), a metabolite of di-butyl phthalate, or by a secondary effect attributed to a hypoxic condition due to the MBP-induced hemoglobin deprivation, the testes were perfused with a solution of MBP in Eagle's MEM or the MEM with/without oxygen, and the activities of testicular enzymes were measured. A decrease in the succinate dehydrogenase (SUDH) activity was observed by the hypoxic perfusate [20-30% dissolved oxygen (DO)], and an induction of apoptosis was observed by the 7% DO perfusate. However, the 100 mM MBP perfusate decreased the activity of SUDH per testis weight, but not per protein level. Therefore, this study proposes that the toxicity might be caused by hypoxia and a coincident depletion of SUDH activity, followed by an apoptotic testicular cell death.
Chlorinated ethylenes (CEs) are known to be metabolized by CYP2C as well as CYP2E1 and CYP2B. The effects of CEs on the expression of the rat CYP2C gene in the liver and lung were comparatively studied in terms of the enzyme activity, and protein and mRNA contents. Tetrachloroethylene (PCE), trichloroethylene (TCE), and 1,1-dichloroethylene (1,1-DCE) were injected at 0.5 g/kg i.p. into male 7-week-old Wistar rats individually or in combination with phenobarbital (PB). The expression of CYP2C mRNA showed organ-specific properties without being detectable in the lung under the assay conditions employed in the present study. Individual CEs had no effect on the enzymatic activity of CYP2C estimated by 2α-hydroxylation of testosterone (2α-TSH), whereas PB markedly enhanced the enzymatic activity in the liver but not the lung microsomes, although it was highly susceptible to the suppressive effect of 1,1-DCE. A down-regulation of pulmonary enzyme activity was observed with PCE by an unknown mechanism when the animals were treated simultaneously with PB. 1,1-DCE was found to inhibit the expression of hepatic mRNA irrespective of the coexistence of PB, and the same was true for CYP2C protein in the same organ to a lesser extent. In an analogy to our previous findings with other xenobiotic-metabolizing CYP forms such as CYP2B1/2 and CYP2E1, a potent suppressive effect of 1,1-DCE was observed with the maximum around 18 hr after the treatment on both constitutive and PB-induced expression of CYP2C.
An assay for the Maillard reaction has been developed to screen efficiently inhibitors from natural resources such as extracts of plants. The fluorometric analysis of fluorescent material based on advanced glycation endproducts (AGEs) was applied to measurement of an inhibitory index of the Maillard reaction to detect all of the inhibitors at each step of the complicated reaction. To solve the two major problems, slowness of the reaction rate and the existence of interfering substances such as quencher and fluorescent material in the screening sources, we devised the following procedures. Slowness of the reaction rate was solved by raising the reaction temperature to 60°C at which the conformation of bovine serum albumin (BSA) did not change greatly. To remove the interfering substances, AGEs-BSA was precipitated from the reaction mixture. Thus, an efficient assay system by measuring the fluorescent intensity based on AGEs was established to isolate the glycation inhibitors from natural product extracts.
It was previously reported that free iron was released from rat red blood cells in both an in vitro study with a metabolite, mono-n-butylphthalate (MBP), of di-n-butylphthalate (DBP) and an in vivo study with oral DBP, inducing rat testicular atrophy in hypoxic conditions due to MBP-induced hemoglobin deprivation. This study investigated whether mono-n-alkylphthalates (alkyl-carbon C4-C6 ; MAP), which result in rat testicular damage, induce iron release from hemoglobin by incubation with rat red blood cells. Iron release was observed with C3-C6 MAP incubation at lower doses and with C1 and C2 MAP incubation at higher doses, but not with C7, C8, and C4(6) MAP.
We hypothesized that participation of sensory neuropeptides, substance P and neurokinin A in the airway inflammation caused to resistance against the glucocorticoids (GCs) treatment. We have measured the expression level of cytokines and chemokines mRNAs in bronchoalveolar lavage cells (BAL), transbronchial lung biopsies (TBLB) and peripheral blood mononuclear cells (PBMC) by reverse transcriptase polymerase chain reaction (RT-PCR). The mRNAs of interleukin-4 (IL-4) and -5, which are typical Thelper 2 (Th2)-type cytokines, were scarcely detected in all of bronchoalvelar lavage fluid (BALF) and TBLB samples. But the mRNA of Th1-type cytokines, such as IL-12, IL-18, and interferon-γ (IFN-γ), tended to be expressed higher than that of Th2-type cytokines at the early stage of asthma before intervention with GCs. The mRNAs of IL-18, IFN-γ, macrophage-derived chemokine (MDC) and thymus- and activation-regulated chemokine (TARC) tended to be expressed higher than that of non-asthmatic subjects. In vitro study demonstrated that the expression of TARC mRNA induced by the combination of IL-4, IFN-γ, and neurokinin A in human bronchial epithelial cells, BEAS-2B was not inhibited by the treatment of the cells with dexamethasone even at 10-6 M. We proposed that the part of resistance to GCs in the asthmatic patient without GC receptor β expression might be associated with the induction of TARC expression in airway epithelial cells by tachykinines and histamine.
The mutagenicity of 255 compounds were examined under the same conditions using the improved Ames test. These compounds were detected frequently in environment, were suspected of high toxicity, or were used as the positive standards for several toxicity tests. The relationships between the chemical structure and the strength of the mutagenicity were analyzed. Thirty compounds of the 255 tested compounds showed mutagenicity. It was found that the compounds, which are unintentionally formed, tended to show mutagenicity in a higher ratio but the artificially synthesized compounds tended to show it in a lower ratio. The number of compounds showed indirect mutagenicity (+S9) were more than the number of compounds showed direct mutagenicity (-S9) in the tested compounds. The mutagenicity strength was different by several hundred thousand times among the compounds. Condensed polycyclic aromatic nitrohydrocarbons, on the whole, showed very strong mutagenicity. The compounds were classified by the positive conditions. All of the tested condensed polycyclic aromatic nitrohydrocarbons accounted for the greatest majority of the compounds which showed mutagenicity under all the conditions of TA98 ± S9 and TA100 ± S9. Only two specific compounds showed mutagenicity under the three conditions except for TA98-S9. Some compounds showed mutagenicity only under the conditions of -S9 but there were various kinds of compounds which showed mutagenicity only under the conditions of +S9. The compounds which showed mutagenicity under only one condition showed weak mutagenicity.
The free-living nematode, Caenorhabditis elegans (C. elegans) was adopted as a multicellular biosensor of biological toxicity from alkylphenols and organotin compounds. Alkylphenols were found to affect reproduction at lower doses than indicated by the acute toxicity assay. In particular, nonylphenol altered the reproduction rate of C. elegans at a dose 10- to 100-fold lower than the 50% lethal concentration (LC50). A comparison of the number of viable worms and eggs suggested that alkylphenols and organotin compounds possess hatching toxicity. A 0.1 μM dose of organotin compounds caused a significant decrease, in the order of 20-50%, in reproduction of the worms, and an abnormal male: hermaphrodite ratio was observed. C. elegans therefore appears to represent a potent and sensitive organism with which to evaluate the biological effects of chemicals. In particular, the sensitivity of reproduction as an endpoint is highly useful for assessing the sublethal effects of chemicals.
The protective effects of an acellular pertussis vaccine were investigated in a murine model of respiratory infection (aerosol challenge model) with various strains of Bordetella pertussis (B. pertussis) as challengers. There were no significant differences in terms of the time course of increases in numbers of bacterial cells in mouse lungs after aerosol challenge among the tested phaseI strains. The vaccine had a strong protective effect against of B. pertussis strain Tohama the phaseI strain used for production of the vaccine, however was less effective against other clinical isolates of pertussis. Our data suggest that a novel vaccine(s) should be developed from the strains derived from current clinical isolates to eliminate the incidence of pertussis.
We measured radioactivity levels of 137Cs and 40K in crude drugs imported from Asian countries by γ-ray spectrometry using Ge detector — MCA. Concentrations of 137Cs in imported crude drugs were very low and close to the limits of detection (about 0.3 Bq/kg dry weight). Furthermore, the type of radioactivity absorbed differed among species. The concentration of 137Cs was high only in ASIASARI RADIX, whereas 40K concentrations were high in herb drugs such as PLANTAGINIS HERBA.
The effects of grape seed polyphenol (GSP) administered orally at doses of 0.01-1.0 g/kg per day to normal and hypercholesterolemic rats for 28 and 36 days, respectively, was evaluated by measuring changes both in the concentrations of serum and hepatic lipids and in fecal steroid excretion. Body weight gain decreased dose-dependently both in normal and hypercholesterolemic rats. Relative weight of the liver was significantly lower in normal rats given more than 0.2 g/kg GSP compared with control rats. Compared with control groups, relative weight of the liver was significantly lower in normal rats given more than 0.2 g/kg GSP, and in hypercholesterolemic rats given more than 0.1 g/kg GSP, respectively. In hypercholesterolemic rats, food or calorie intake was significantly lower in rats given more than 0.1 g/kg GSP than in control rats. Dose-dependency was observed in serum concentrations of serum triglycerides and thiobarbituric acid reactive substances and the content of hepatic phospholipids in normal rats, and in serum concentration and hepatic content of triglycerides in hypercholesterolemic rats. A significant increase in fecal excretions of neutral steroids and bile acids was found in normal rats given a dose of 1.0 g/kg GSP. Dose-dependent decrease of 12-keto lithocholic acid and increase of lithocholic acid were also observed. By contrast, there was no significant change in fecal excretions of neutral steroids and bile acids in hypercholesterolemic rats. Thus, GSP seems to affect lipid metabolism in rats by lowering the concentrations of serum and hepatic triglycerides rather than by altering the metabolism of cholesterol.
Placental transfer of bisphenol-A (BPA) was studied in mice and Japanese monkeys (Macaca fuscata). BPA was found in maternal and fetal sera, liver, brain, uteri, testes and placenta as early as 30 min after a single subcutaneous (s.c.) injection to 17 days of pregnancy in mice. BPA was also found in fetal liver, kidney, and brain of Japanese monkeys 1 hr after a single s.c. injection to 150 days of pregnancy. These results clearly indicate that the maternal placental barrier can not protect the fetus from the consequences of BPA exposure in these species.
To evaluate the toxicity of environmental chemicals to invertebrates, a static bioassay was developed in the laboratory using the Caenorhabditis elegans (C. elegans). First, reproducibility of this aquatic acute toxicity test system was confirmed. In order to estimate chemical toxicities in C. elegans, worms were subsequently exposed to eleven different xenobiotics. Mortality after 24 hr was adopted as the endpoint of toxicity. We found that benzo[a]pyrene, nonylphenol, benzophenone, bisphenol A and cadmium chloride affected viability of C. elegans. These data suggest that C. elegans is a suitable toxicity test organism for environmental xenobiotic chemicals, and that lethality can be used as a testing endpoint.
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