The Role of Lipids in Enhancing the Koku Perception of Pork Sausage.

This study was investigated the effect of adding fat to pork sausage on taste and aroma persistence. Sensory evaluation indicated that increasing fat content intensified umami and saltiness perception, enhancing the mouthfulness and flavor persistence, leading to Koku enhancing effect. Gas chromatography/mass spectrometry (GC/MS) analysis identified aroma compounds such as ß-pinene, 3-carene, D-limonene, octanal, nonanal, caryophyllene, and methyl eugenol, which were consistently present regardless of fat content. These aroma compounds were less likely to be released as the fat content increased. Furthermore, the release of these aroma compounds from the sausage with addition of fat was larger than that without addition of fat in the presence of saline, indicating that the added fat retained these aroma compounds and released them in the presence of saline. This suggests that sausages with added fat release more aroma compounds during consumption, resulting in a more intense flavor and flavor persistence of Koku perception. These seven compounds detected in pork sausage were found to be easily retained by cholesterol and lecithin, likely due to differences in their log P values (octanol/water partition coefficients), which were greater than 3.

Mutation in Smek2 regulating hepatic glucose metabolism causes hypersarcosinemia and hyperhomocysteinemia in rats.

Suppressor of mek1 (Dictyostelium) homolog 2 (Smek2), was identified as one of the responsible genes for diet-induced hypercholesterolemia (DIHC) of exogenously hypercholesterolemic (ExHC) rats. A deletion mutation in Smek2 leads to DIHC via impaired glycolysis in the livers of ExHC rats. The intracellular role of Smek2 remains obscure. We used microarrays to investigate Smek2 functions with ExHC and ExHC.BN-Dihc2BN congenic rats that harbor a non-pathological Smek2 allele from Brown-Norway rats on an ExHC background. Microarray analysis revealed that Smek2 dysfunction leads to extremely low sarcosine dehydrogenase (Sardh) expression in the liver of ExHC rats. Sarcosine dehydrogenase demethylates sarcosine, a byproduct of homocysteine metabolism. The ExHC rats with dysfunctional Sardh developed hypersarcosinemia and homocysteinemia, a risk factor for atherosclerosis, with or without dietary cholesterol. The mRNA expression of Bhmt, a homocysteine metabolic enzyme and the hepatic content of betaine (trimethylglycine), a methyl donor for homocysteine methylation were low in ExHC rats. Results suggest that homocysteine metabolism rendered fragile by a shortage of betaine results in homocysteinemia, and that Smek2 dysfunction causes abnormalities in sarcosine and homocysteine metabolism.

SLIM1 Transcription Factor Promotes Sulfate Uptake and Distribution to Shoot, Along with Phytochelatin Accumulation, Under Cadmium Stress in Arabidopsis thaliana.

Sulfur (S) assimilation, which is initiated by sulfate uptake, generates cysteine, the substrate for glutathione (GSH) and phytochelatin (PC) synthesis. GSH and PC contribute to cadmium (Cd) detoxification by capturing it for sequestration. Although Cd exposure is known to induce the expression of S-assimilating enzyme genes, including sulfate transporters (SULTRs), mechanisms of their transcriptional regulation are not well understood. Transcription factor SLIM1 controls transcriptional changes during S deficiency (-S) in Arabidopsis thaliana. We examined the potential involvement of SLIM1 in inducing the S assimilation pathway and PC accumulation. Cd treatment reduced the shoot fresh weight in the sulfur limitation1 (slim1) mutant but not in the parental line (1;2PGN). Cd-induced increases of sulfate uptake and SULTR1;2 expressions were diminished in the slim1 mutant, suggesting that SLIM1 is involved in inducing sulfate uptake during Cd exposure. The GSH and PC levels were lower in slim1 than in the parental line, indicating that SLIM1 was required for increasing PC during Cd treatment. Hence, SLIM1 indirectly contributes to Cd tolerance of plants by inducing -S responses in the cell caused by depleting the GSH pool, which is consumed by enhanced PC synthesis and sequestration to the vacuole.

Plants prioritize phytochelatin synthesis during cadmium exposure even under reduced sulfate uptake caused by the disruption of SULTR1;2.

Glutathione and phytochelatins are sulfur containing compounds playing an important role in cadmium (Cd) detoxification. We examined the Cd-induced changes in the percentage of sulfur containing compounds to total sulfur in wild-type and sulfate transporter 1;2 knockout mutant, sel1-10. Cd treatment increased the proportion of sulfate and thiols in the total sulfur content. Among the thiols analyzed, the proportion of cysteine and glutathione were decreased by the Cd treatment and that of the phytochelatins were increased. Although the total sulfur content in sel1-10 was decreased compared with that in wild-type, the percentages of individual thiol in the total thiol content were similarly maintained between sel1-10 and wild-type, suggesting that plants tightly controlled the balance of each thiol under Cd treatment.

Effects of Cadmium Treatment on the Uptake and Translocation of Sulfate in Arabidopsis thaliana.

Cadmium (Cd) is a highly toxic and non-essential element for plants, whereas phytochelatins and glutathione are low-molecular-weight sulfur compounds that function as chelators and play important roles in detoxification. Cadmium exposure is known to induce the expression of sulfur-assimilating enzymes and sulfate uptake by roots. However, the molecular mechanism underlying Cd-induced changes remains largely unknown. Accordingly, we analyzed the effects of Cd treatment on the uptake and translocation of sulfate and accumulation of thiols in Arabidopsis thaliana Both wild type (WT) and null mutant (sel1-10 and sel1-18) plants of the sulfate transporter SULTR1;2 exhibited growth inhibition when treated with CdCl2 However, the mutant plants exhibited a lower growth rate and lower Cd accumulation. Cadmium treatment also upregulated the transcription of SULTR1;2 and sulfate uptake activity in WT plants, but not in mutant plants. In addition, the sulfate, phytochelatin and total sulfur contents were preferentially accumulated in the shoots of both WT and mutant plants treated with CdCl2, and sulfur K-edge XANES spectra suggested that sulfate was the main compound responsible for the increased sulfur content in the shoots of CdCl2-treated plants. Our results demonstrate that Cd-induced sulfate uptake depends on SULTR1;2 activity, and that CdCl2 treatment greatly shifts the distribution of sulfate to shoots, increases the sulfate concentration of xylem sap and upregulates the expression of SULTRs involved in root-to-shoot sulfate transport. Therefore, we conclude that root-to-shoot sulfate transport is stimulated by Cd and suggest that the uptake and translocation of sulfate in CdCl2-treated plants are enhanced by demand-driven regulatory networks.

Paralytic toxicity in the ribbon worm Cephalothrix species (Nemertea) in Hiroshima Bay, Hiroshima Prefecture, Japan and the isolation of tetrodotoxin as a main component of its toxins.

Paralytic toxicity of ribbon worms ("himomushi" in Japanese), identified as undescribed species of the genus Cephalothrix, found on the surface of the shells of cultured oysters in Hiroshima Bay, Hiroshima Prefecture was examined between April 1998 and December 2001. The toxicity study showed that all of specimens were found to contain toxins with strong paralytic action in mice; the highest toxicity (as tetrodotoxin, TTX) was 25,590 mouse units (MU) per gram for whole body throughout the monitoring period. The main toxic component of this himomushi toxin (HMT) was isolated from a pooled specimen (390 g; total toxicity 2,897,000MU) by a method that consisted of treatment with activated charcoal, chromatography on Bio-Gel P-2 and Bio-Rex 70 (H+ form), and finally crystallization from an acidified methanolic solution. The recrystallized toxin showed a specific toxicity of 3520MU/mg. This toxin showed (M+H)+ and (M+H-H(2)O)+ ion peaks at m/z 320 and 302, respectively, by electrospray ionization-mass spectrometry (ESI-MS). The absorption band at 3353, 3235, 1666, 1612 and 1076 cm(-1) were observed in infrared spectrum of this toxin. This spectrum was indistinguishable from that of TTX. The 1H-NMR spectrum for the recrystallized toxin was the same as that for TTX. The pair of doublets centered at 2.33 (J=10.0Hz) and 5.48 ppm (J=10.0Hz) which are characteristic of TTX, were shown to be coupled by double irradiation. Furthermore, by gas chromatography-mass spectrometry (GC-MS) of the alkali-hydrolyzate of this toxin indicated the presence of quinazoline skeleton (C9-base) specific to TTX.

Twenty-six week carcinogenicity study of ampicillin in CB6F1-TgrasH2 mice.

As a part of the ILSI-HESI Alternative to Carcinogenicity Testing (ACT) program, we performed a 26-week carcinogenetic study of nonmutagenic drug, ampicillin (ABPC) in Tg-rasH2 mice. ABPC was given to Tg-rasH2 mice (0, 350, 1000, 3000 mg/kg, p.o.) and Non-Tg mice (0, 3000 mg/kg, p.o.) daily for 26 weeks. As a positive control, a single dose of MNU was administered once to Tg-rasH2 mice (75 mg/kg, i.p.). In this study, Tg-rasH2 mice did not demonstrate any increases in tumor development in response to ABPC. Thus, ABPC had no carcinogenicity in the 26-week carcinogenesis study in Tg-rasH2 mice or in a 2-year carcinogenesis study in B6C3F1 mice.