• Title/Summary/Keyword: Maki

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Different Regulation of p53 Expression by Cadmium Exposure in Kidney, Liver, Intestine, Vasculature, and Brain Astrocytes

  • Lee, Jin-Yong;Tokumoto, Maki;Hattori, Yuta;Fujiwara, Yasuyuki;Shimada, Akinori;Satoh, Masahiko
    • Toxicological Research
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    • v.32 no.1
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    • pp.73-80
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    • 2016
  • Chronic exposure to cadmium (Cd) is known to adversely affect renal function. Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells. In this study, the effects of Cd on protein expression of p53 and apoptotic signals in the kidney and liver of mice exposed to Cd for 12 months were examined, as well as the effects of Cd on p53 protein levels and gene expression of the Ube2d family in various cell lines. Results showed that in the kidney of mice exposed to 300 ppm Cd for 12 months, there was overaccumulation of p53 proteins in addition to the induction of apoptosis, which was triggered specifically in the proximal tubules. Interestingly, the site of apoptosis was the same as that of p53 accumulation in the proximal tubules. In the liver of mice chronically exposed to Cd, gene expression of the Ube2d family tended to be slightly decreased, together with slight apoptosis without the accumulation of p53 protein. In rat small intestine epithelial (IEC-6) cells, Cd decreased not only the p53 protein level but also gene expression of Ube2d1, Ube2d2 and Ube2d4. In human brain microvascular endothelial cells (HBMECs), Cd did not suppress gene expression of the Ube2d family, but increased the p53 protein level. In human brain astrocytes (HBASTs), Cd only increased gene expression of UBE2D3. These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.

Inactivation of Pathogenic Bacteria by Addition of Thermophilic Bacteria in the Thermophilic Aerobic Oxidation(TAO) System (고온호기산화장치의 고온미생물 첨가에 의한 병원성 미생물의 불활성화)

  • Lee W. I.;H. Tsujii;T. Maki;Lee M. G.
    • Journal of Animal Environmental Science
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    • v.10 no.2
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    • pp.111-118
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    • 2004
  • This study analyzed temperature increase, microorganism changes, and inactivation of pathogenic microorganisms in pig slurry when treated with thermophilic microorganisms in Thermophilic Aerobic Oxidation(TAO) system. An amount of $6 m^3$ of pig slurry was treated in an $18 m^3(3.0\times2.5\times2.4 m)$ reactor for 5 to 7 days in two groups: the control of pig slurry only and the treatment of pig slurry with 6 liters of thermophilic microorganism(Bacillus sp.). To study the microorganism changes in the reactor, the populations of aerobic mesophilic microorganisms, thermophilic microorganisms and general pathogens were analyzed. To study the inactivation of pathogenic microorganisms, the levels of E. coli, Salmonella sp, Crytosporidium parvum and Giardia lamblia were analyzed. The temperature inside the reactor ranged from 18 to $62^{\circ}C$ for the control while far the treatment group it ranged from 18 to $66^{\circ}C$, showing a slightly higher array. With regard to changes in microorganisms, both mesophilic and thermophilic organisms decreased from $3.1\times10^6$ to $1.2\times10^2$ CFU/ml and from $1.0\times10^4$ to $8.0\times10^1$ CFU/ml, respectively, in the control. In the treatment, on the other hand, mesophilic organisms decreased from $3.0\times10^8$ CFU/ml to $8.6\times10^5$ CFU/ml while thermophilic organisms increased sharply from $2.0\times10^6$ to $1.2\times10^8$ CFU/ml. For pathogens, Salmonella and Giardia were not detected either before or after the treatment, while E. coli and C. parvum were found to be $10^5$ CFU/ml each before treatment and negative after it. From this experiment, it was concluded that thermophilic microorganisms could effectively sanitize liquid compost by generating high temperature in the TAO system, which in turn would inhibit the growth of pathogenic organisms.

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