Influence of Milk on Exhaled Carbon Monoxide (CO) Measurement by Portable CO Monitors.

Background: A portable breath carbon monoxide (CO) monitor has a high cross-sensitivity to hydrogen (H2). This study examined the influences of H2 after consuming milk on the detected CO values using three types of portable CO monitors. Materials and Methods: Exhaled breath from seven participants (four healthy nonsmokers and three smokers with otherwise unknown comorbidities) was collected in sampling bags. The participants then consumed 200 mL of milk, and the exhaled breath of each was collected in separate bags every 30 minutes until 9 hours later. CO and H2 in the bag were measured using a gas chromatograph as a reference analyzer, and CO was also measured using three types of portable CO monitors. Results: After consuming milk, H2 levels were significantly higher, and CO levels were not significantly elevated as measured by the reference analyzer. However, CO levels in monitors A and B were significantly elevated, even though participants did not smoke. The H2 levels in the reference analyzer significantly increased and reached a maximum 4.5 hours after consuming milk. The difference in CO levels between the reference analyzer and each monitor increased significantly after 5 or 5.5 hours. Conclusions: This study suggested that the breath CO monitors with a cross-sensitivity to H2 responded to H2 as CO in the exhaled gas and measured higher than actual values after milk consumption. The extent of the influence of H2 differed depending on the type of CO monitor. It is necessary to consider milk consumption when assessing the smoking status of people using portable CO monitors.

Effects of butyltin compounds on mitochondrial respiration and its relation to hepatotoxicity in mice and Guinea pigs.

Because the mechanisms responsible for the difference in toxicity between different experimental animal species remain unclear, the effects of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) on mitochondrial respiration were compared among the livers of mice and guinea pigs in vitro and in vivo. Further, the levels of these butyltin compounds and their derivatives in the mitochondrial fractions of the hepatocytes were investigated in these animal species. Administration of TBTC and DBTC to mice resulted in the obvious elevation of serum enzymatic activities, as well as the inhibition of succinate-linked State 3 respiration in hepatic mitochondria at 24 h after administration. On the other hand, these metal compounds failed to induce such hepatotoxicity or to inhibit mitochondrial respiration in guinea pigs. There was no significant difference between mice and guinea pigs in the IC50 (metal concentration observed in 50% inhibition of mitochondrial respiration) of TBTC and DBTC against the succinate-linked State 3 respiration of hepatic mitochondria in vitro, although the mitochondrial respiration of succinate-linked State 3 was inhibited in the liver of mice treated with the metals in vivo. The levels of total butyltin compounds in the mitochondrial fractions of hepatocytes were higher in the mice than in the guinea pigs, and the main butyltin compound in the mitochondrial fractions was DBTC in both species at 24 h after TBTC or DBTC administration. The amount of sulfhydryl groups, which were capable of binding with DBTC, in mice hepatic mitochondria was twice as large as that in guinea pigs, and the affinity of DBTC for the isolated hepatic mitochondria was higher in mice than in guinea pigs in vitro. These results suggested that the induction of hepatotoxicity by TBTC and DBTC in vivo was closely associated with the depression of mitochondrial respiration and that the difference in susceptibility to the metal-induced mitochondrial damages between mice and guinea pigs might result from the high affinity of butyltin compounds, in particular DBTC, for hepatic mitochondria in mice containing higher levels of sulfhydryl groups, compared with guinea pigs.

DNA microarray analysis of genomic responses of yeast Saccharomyces cerevisiae to nickel chloride.

In order to investigate nickel toxicity against the yeast Saccharomyces cerevisiae, genomic responses to nickel chloride were examined using yeast DNA microarrays. Microarray analysis revealed that exposure to 25 mM nickel chloride for 2 hr induced changes in gene expression in S. cerevisiae. Nickel chloride increased expression levels in 601 genes and decreased expression levels in 696 genes in S. cerevisiae.

[Combined estrogenic activity of soybean extract used in a dietary supplement and ethinyl estradiol].

We examined the combined estrogenic activity of soybean extract used in a dietary supplement and ethinyl estradiol (EE) contained in an oral contraceptive. Olive oil (control), soybean extract (0.0036 or 0.36 g/kg corresponding to doses of total isoflavone of 0.83 or 83 mg/kg respectively), EE (1 or 10 microg/kg), and soybean extract+EE were administered to ovariectomized CD-1 mice by oral gavage for 4 consecutive days. Soybean extract (0.0036 or 0.36 g/kg) and EE (1 microg/kg) did not increase the relative uterine weight. The relative uterine weight of the soybean extract (0.0036 or 0.36 g/kg)+EE (10 microg/kg) group was significantly higher than that of the control. The relative uterine weight of the soybean extract (0.36 g/kg)+EE (10 microg/kg) group was also significantly higher than that of the EE (10 microg/kg) group. Soybean extract showed estrogenic activity for human estrogen receptor (hER)-alpha and -beta. Coadministration of EE with soybean extract increased the estrogenic activity for hER-alpha and -beta.

Oral administration of acidic xylooligosaccharides prevents the development of atopic dermatitis-like skin lesions in NC/Nga mice.

We examined whether two types of xylooligosaccharides (neutral or acidic xylooligosaccharides) derived from hardwood kraft pulp ameliorate the development of atopic dermatitis (AD)-like skin lesions induced by repeated application of picryl chloride (PiCl) in NC/Nga mice. Oral administration of acidic xylooligosaccharides at a daily dose of 100 mg/kg significantly prevented the development of AD-like skin lesions. Serum histamine level was significantly suppressed, but serum total IgE level was not significantly suppressed. Moreover, the secretion of inflammatory cytokine IL-12 from splenic lymphocytes was significantly suppressed. On the other hand, neutral xylooligosaccharides showed no significant preventive effect on the development of AD-like symptoms. These results suggest that oral administration of acidic xylooligosaccharides may be effective in preventing the development of AD-like skin disease and one of the mechanisms is the suppressive effect on IL-12.