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Volume 196 (2002)
- Issue 4 Pages 219-
- Issue 3 Pages 99-
- Issue 2 Pages 53-
- Issue 1 Pages 1-
Volume 196, Issue 1
January
Displaying 1-6 of 6 articles from this issue
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Reviews
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SATOMI ONOSAKA, NORIKO TETSUCHIKAWAHARA, KYON-SON MIN2002 Volume 196 Issue 1 Pages 1-7
Published: 2002
Released on J-STAGE: April 19, 2004
JOURNAL FREE ACCESSZinc (Zn) is an essential, common metal in animal tissues. Zn levels were elevated in only four tissues after Zn administration, the highest increase being in the pancreas. Zn concentration was increased by metallothionein induction. Metallothionein-bound Zn significantly reduced the toxicity of the metals Cd, Cu and Hg. It should be noted that tissue Zn levels are different in experimental animals and humans. Acute pancreatitis was observed following the injection of a large dose of Zn. Different metals have different target organs. Using metal pathology, treatments may be developed to save patients suffering from hepatic and renal diseases because Zn is used to a model animal of hepatic or renal disease.View full abstractDownload PDF (2312K) -
MASAO SATO, MASUO KONDOH2002 Volume 196 Issue 1 Pages 9-22
Published: 2002
Released on J-STAGE: April 19, 2004
JOURNAL FREE ACCESSMetallothionein (MT) is a ubiquitous, cysteine-rich, metal-binding protein. MT synthesis is induced by various stimuli such as cadmium, mercury, zinc, oxidative stress, glucocorticoid, and anticancer agents. Recently, transgenic mice with loss-of-function mutations in the MT-I/-II genes were established. It has been assumed that MT plays a role in the detoxification of heavy metals. In recent studies using MT-null mice, the ability of MT to protect against cadmium-induced renal, liver and bone injuries has been confirmed. Moreover, MT is also capable of scavenging oxygen free radicals. MT is involved in the protection of tissues against various forms of oxidative injury, including radiation, lipid peroxidation, oxidative stress caused by anticancer drugs, and conditions of hyperoxia. However, MT still lacks an established biological function. Unexpectedly, the MT-null mice were apparently in good health, and the critical biological roles of MT have been questioned. MT seems to be a protective protein produced in response to a variety of stresses. Here, current studies on the protective roles of MT against toxicity of heavy metals and reactive oxygen species are reviewed, and the putative biological functions of MT are discussed.View full abstractDownload PDF (937K) -
MASAHIKO SATOH, HIROSHI KOYAMA, TOSHIYUKI KAJI, HIDEAKI KITO, CHIHARU ...2002 Volume 196 Issue 1 Pages 23-32
Published: 2002
Released on J-STAGE: April 19, 2004
JOURNAL FREE ACCESSSince there are a plethora of studies on cadmium toxicity and poisoning in laboratory animals and humans, we have limited this review to studies that are relevant to human health issues by focusing on carcinogenicity, genotoxicity, circulatory disease, nephrotoxicity and life expectancy. Cadmium exposure has been established to induce cancer in various tissues of laboratory animals. Contrary to early findings of the lack of genotoxicity by cadmium, recent findings of mammalian cell culture studies have revealed genotoxic effects. Furthermore, cadmium exposure at relatively low doses induces circulatory diseases in laboratory animals. Despite such results of various cadmium toxicities in animal studies, data from human studies are lacking and insufficient to support the cause-effect relationship. Although cadmium is currently considered to be a human carcinogen by the International Agency for Research and Cancer, it is inappropriate to conclude that sufficient evidence on the carcinogenicity of cadmium in humans exists. It is also thought that epidemiological studies so far reported do not support the occurrence of cadmium-induced circulatory disease in humans. Since there are inconsistent reports on the relationship of cadmium exposure with the life expectancy of people living in cadmium-polluted areas, further studies are needed for clarification. It is also necessary to examine apparent discrepancies in result between humans and experimental animals. It has been established that long-term exposure to cadmium causes renal dysfunction in both humans and experimental animals, and whether there are any differences in the inducibility of metallothionein in the kidney warrants further study.View full abstractDownload PDF (688K) -
HISAYOSHI OHTA, MASAYO ICHIKAWA, YUKIO SEKI2002 Volume 196 Issue 1 Pages 33-42
Published: 2002
Released on J-STAGE: April 19, 2004
JOURNAL FREE ACCESSCadmium (Cd) is a heavy metal that exists ubiquitously in the environment, and it interacts with essential elements such as zinc, copper, iron, and calcium (Ca). Particularly, Cd interferes with Ca and vitamin D metabolism in bone kidney and intestine. The interaction between Cd and Ca in bone, intestine, and kidney may result in the disorder of bone metabolism. On the other hand, pregnancy and lactation are also important physiological factors affecting bone metabolism in the mother. Ca absorption is decreased by competition with Cd in the intestine, and more Ca is released from maternal bone and transferred to neonate by lactation. In the intestine, Cd uptake competes with Ca uptake. Cd causes a marked decrease in bone density compared to the normal decrease in bone mineral density during lactation. Lactation is an important factor contributing to the decrease in bone mineral density and Cd has an additive effect of decreasing bone metabolism of mother animal, although the Cd intake level is relatively low (approximately 3-14 μgCd/kg/day). The relationship among maternal Cd intake, renal function and bone metabolism and the interaction between Cd and Ca during lactation are reviewed herein, together with additional data obtained recently in our laboratory.View full abstractDownload PDF (697K) -
SEIICHIRO HIMENO, TAKAHIRO YANAGIYA, SHUICHI ENOMOTO, YUKIHIRO KONDO, ...2002 Volume 196 Issue 1 Pages 43-50
Published: 2002
Released on J-STAGE: April 19, 2004
JOURNAL FREE ACCESSThe mechanism of cellular cadmium (Cd) uptake has been poorly understood. Recently, we developed Cd-resistant cell lines from metallothionein null mouse cells and showed that the Cd resistance of these cells was conferred primarily by a reduced Cd accumulation. Surprisingly, the uptake rate of manganese (Mn) was also markedly reduced in Cd-resistant cells. Subsequent studies on the kinetics of Cd and Mn uptake by Cd-resistant and parental cells revealed that the Mn transport system with high affinity for Mn is used for cellular Cd uptake, and that this pathway is suppressed in Cd-resistant metallothionein null cells. This is the first indication that the transport system for Mn is used for Cd uptake in mammalian cells. Divalent metal transporter 1 (DMT1) is the only known mammalian transporter involved in the uptake of both Cd and Mn. However, the high-affinity Mn/Cd transport system we found seems to be distinct from DMT1 because of the difference in optimal pH and substrate specificity. On the other hand, various types of Mn transporters have been shown to play an important role in cellular Cd uptake in non-mammalian species such as yeast, plants and bacteria, suggesting the existence of Mn transporters other than DMT1 in mammals.View full abstractDownload PDF (588K)
Retraction
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YOHICHI SEINO, RYUKO ITO, ICHIRO SUZUKI, KEIJI ENZAN, HIDEO INABAArticle type: Others
Subject area: Others
2002 Volume 196 Issue 1 Pages 51
Published: 2002
Released on J-STAGE: April 05, 2005
JOURNAL FREE ACCESSRetracted Publication
Yohichi Seino, Ryuko Ito, Ichiro Suzuki, Keiji Enzan and Hideo Inaba. A Utstein-Style Analysis of Prognostic Factors Related to Survival in Out-of-Hospital Cardiac Arrests in Akita-City, Japan. Tohoku J. Exp. Med., 2001, 194(2), 107-119.
In previous publication in the Tohoku Journal of Experimental Medicine, we reported the “Out-of-Hospital Cardiac Arrests in Akita.” After publication of the paper, we have become aware of a crucial error in the sampling of the patients. The conclusion based on such incorrectly obtained data may cause serious confusions in the field of emergency medicine. We therefore wish to retract the above paper.View full abstract
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