In recent years, the number of patients visiting outpatient clinics with complaints of abnormal sense of taste and/or olfaction has been on the increase. It has been estimated that about 30% of these patients may have dietary zinc deficiency. This deficiency is more likely to develop among children whose the daily requirement of zinc is greater, among elderly people whose dietary consumption of nutrients is poor and among young women who are often on diets for weight reduction. Zinc deficiency may be associated with a variety of features such as hypogeusia, hyposmia, growth retardation, dermatitis, alopecia, compromised gonadal functions, susceptibility to infections and delayed wound healing. This manuscript reviews zinc physiology (distribution in the body, absorption, transport, metabolism and excretion, physiological functions and factors causing changes in the serum level) and zinc supplementary therapy for better understanding of the clinical features of zinc deficiency.

抄録全体を表示

The number of patients with taste disorders are remarkably increasing. There are many causes of taste disorders, and accordingly their clinical states are various. Of these disorders, those found frequently are secondary taste disorders, which occur as a result of zinc deficiency or medication for treatment of other diseases. The mechanism of occurrence of taste disorders has been studied in association with zinc, one of trace elements. In this article, causes of taste disorders are described mainly in connection with zinc. In addition, zinc therapy, which has been examined relatively objectively heretofore, is evaluated. Usefulness of zinc administration for taste disorder has been expressed.

抄録全体を表示

We evaluated zinc concentrations in patients with hepatitis C virus (HCV)-positive chronic liver disease and correlated them with the clinical profiles of the patients. 11 healthy subjects also were included in this study. Serum zinc concentrations were evaluated using conventional atomic absorption spectrometry. The median concentration of zinc in patients with CH was statistically lower than that in healthy control subjects. The median zinc concentrations of the LC and HCC groups were significantly lower than that of the CH group. A significant correlation was observed between the zinc concentrations and the platelet counts and albumin concentrations. The zinc concentrations did not correlate with tumor size and number and decreased with the development of Child-Pugh stage. The zinc concentrations did not correlate with tumor size and number and decreased with the development of Child-Pugh stage. The cumulative survival rate after therapy for HCC nodules in the low zinc concentration group was significantly lower than in the high group.We concluded the serum concentration of zinc influenced the clinical profiles in patients with C-viral chronic liver disease.

抄録全体を表示

Zinc is an essential trace element that is abundantly present in the brain. In spite of its importance for normal brain functions, it is widely recognized that excess zinc is neurotoxic. Numerous studies have indicated that zinc is crucial for neuronal injury after transient global ischemia and is linked with the pathogenesis of vascular type of dementia. We have investigated the molecular mechanisms of zinc-induced neurotoxicity in vitro and have explored substances that protect zinc-induced neurotoxicity. Pharmacological evidence based on results of our own and numerous other studies has indicated the significance of Ca²⁺ dyshomeostasis in the mechanism of zinc-induced neuronal injury. The introduction of zinc into neurons is reportedly mediated through several types of Ca²⁺-permeable channels. Ca²⁺ channel blockers attenuate zinc-induced neurotoxicity. Furthermore, calcium overload attenuates zinc neurotoxicity, and vice versa. In this paper, we review the routes of zinc entry and mechanisms of zinc-induced neuronal death in relation with calcium homeostasis. The possible role of carnosine (β-alanyl histidine), a dipeptide that is present in the brain, as an endogenous protective substance for neuronal injury is also discussed.

抄録全体を表示

Recently, As pollution was reported in groundwater from the Red River delta of Northern Vietnam and the Mekong delta of Southern Vietnam and Cambodia. Although the health of about 10 million people is at risk from the drinking tube well water, little information is available on the health effects of As exposure in the residents of these regions. Also, the countrywide survey on regional distribution of As pollution has not been conducted in these countries. At present, as far as we know, symptoms of chronic As exposure have not yet been reported, probably due to the relative short-term usage of the tube wells in the regions. However, oxidative DNA damage was observed in the residents of Cambodia and so further continuous usage of the tube well might cause severe damage to the health of the residents. In this article, we review literature concerning As pollution of groundwater and its health effects on residents in Vietnam and Cambodia. The mechanisms of As release to the groundwater is also discussed.

抄録全体を表示

This review includes the following topics:(1) A historical sketch of researches on trace elements, which are now at dawn of the new age, was given briefly. (2) Comments and interpretations were given on trends and changes in nutritional requirements of iron, zinc and copper by recommended dietary allowance and dietary reference intakes for Japanese. (3)Discussion was made on intake amounts of iron, zinc and copper by national health and nutrition survey in Japan. In 2003, it is calculated that the population ratio of intake amounts less than estimated average requirements was highest (80%) in iron intake of female followed by iron intake of male and zinc intake of male and female(about 30%) and was lowest (less than 5%) in copper intake of male and female in the age group 30∼49.
Generally, there is a tendency that requirements, estimated intake amounts, normal levels in blood or serum and the content of foods in regard to trace elements have been decreased year by year as a consequence of the development and improvement of analytical methods.

抄録全体を表示

1. In Japan, patients with taste disorder as a primary symptom of zinc deficiency are increasing.
2. The incidence of taste disorder due to diet (insufficient intake of zinc) is especially high. The serum zinc value in patients with taste disorder due to diet was 20μg/dl (in many cases mean value is 60-79μg/dl )lower than the healthy group, but the half cases remained in more than 80μg/dl.
3. The efficacy of oral administration of zinc in patients with taste disorder due to diet did not correlate with the zinc value before this therapy, but about 85%.
4. Increasing rate of serum zinc values after the oral zinc therapy in patients with taste disorder due to diet was significantly high more than the placebo group. Lower serum zinc values in the patients were more effective. Correlate with the amount of oral administration of zinc.
5. We would like to propose 80μg/dl as the diagnosis value(cutoff value) of zinc deficiency, referring to the above results and the conclusion of the Yokoi's study(Association between plasma zinc concentrations and zinc kinetic parameters in premenopausal women).

抄録全体を表示

Toxicity and bioavailability of arsenic strongly depend on its chemical forms. Chemical speciation analysis of arsenic is getting more and more important to clear exactly the characteristics of arsenic, especially organic arsenicals, in vivo and environment. In this review, the present status of analytical methods for speciation of organic arsenicals is described. Potentiality of liquid chromatography combined with inductively coupled plasma mass spectrometry (LC-ICPMS), especially LC-ICPMS using photooxidation and vaporization techniques for high-sensitive speciation analyses of ultra-trace organic arsenicals, is also described.

抄録全体を表示

Au (gold) is a heavy metal and its complexes are one of the more effective medicaments available for rheumatoid arthritis, although many authors have reported serious kidney damage during the chrysotherapy. In this article, the mechanisms of the DNA damage in renal kidney of rats after Au injection are reviewed. Cu content in the kidney of the Au-injected rat dramatically increased in comparison with Au and Zn content and that Cu-binding metallothionein (MT) was predominantly observed in the outer stripe of the outer medulla in the kidney. The signals of terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) and the immunoreactivity of 8-hydroxydeoxyguanosine (8-OHdG) were located in the cortex of the Au-injected rat. Cu detected by Timm's method was mainly distributed in the cortex of Au-injected rat. These findings suggested that the oxidative DNA damage in the kidneys of rats injected with Au is associated with Cu of the cortex except Cu-MT. I postulate that the DNA cleavage might be caused by hydroxyl radicals formed by a monovalance of copper.

抄録全体を表示

Cadmium nitrate (Cd(NO₃)₂; CdN) is commonly used in Ni-Cd battery factories. However, there are few reports regarding the kinetics of CdN. This study was designed to investigate the early dynamic state of Cd in the blood, bile, and urine in rats as a model of accidental occupational exposure to CdN. It was also designed to determine the relationship between the kinetics and harmful effects of CdN. To evaluate the kinetics of CdN exposure and metabolism, rats received a single intravenous injection of CdN (2.1, 4.2, or 6.3 mg/kg). Serum Cd concentrations were determined 0, 5, 10, 30, 60, 120, and 300 min after the injection. Calculating the elimination data of Cd from serum required two-compartment modeling. Bile was collected at intervals of 30 min until 300 min. Urine was collected for 300 min. T_1/2 β, MRT and AUC_0→300 were significantly longer, and the total body clearance, V₁ and V_ss were significantly lower in the 6.3 mg/kg group than those in the other groups. Total biliary and urinary Cd excretion levels were higher in the 6.3 mg/kg group than those in the other groups. Our previous study indicated that acute exposure to CdN causes severe liver and proximal tubular damage, particularly at a dose of 6.3 mg/kg. Abnormalities in Cd kinetics could result from extensive hepatic dysfunction at a toxic dose. This dysfunction could lead CdN to sensitive cellular targets, such as the kidneys, over long periods of time. Kinetics abnormalities and liver and kidneys dysfunctions may enhance CdN toxicity.

抄録全体を表示

Wilson disease is an autosomal recessive disorder of copper metabolism. The disease phenotype includes chronic liver disease (cirrhosis), neurological impairment (extra pyramidal signs), Kayser-Fleischer ring and others. Some patients show psychiatric symptoms. In this paper, we report two patients with Wilson disease who presented with atypical psychiatric symptoms as first symptoms. They presented with hallucination as the initial symptom and were diagnosed with schizophrenia. Several years later, typical neurological symptoms of Wilson disease appeared. The most common psychiatric symptoms are mental retardation and depression in Wilson disease; hallucination is a rare symptom. The clinical courses of these patients were atypical of this disease. Thus, the diagnosis of Wilson disease was unsuspected until they developed obvious symptoms, and a long time was needed to reach the final diagnosis. We should suspect Wilson disease and screen for it in patients with psychiatric symptoms.

抄録全体を表示

Wilson disease is an autosomal recessive disorder of the copper (Cu) metabolism, which is caused by mutations in the ATP7B gene. Wilson disease is treatable, but the delay of its diagnosis will make the treatment more difficult. The establishment of an analytical method for early diagnosis is a very important for early treatment. Usually, 95% of plasma Cu is bound to ceruloplasmin in blood serum and excreted into the bloodstream in the form of Cu-bound protein (holo-ceruloplasmin) in normal subjects. In the case of Wilson disease patients, ceruloplasmin is excreted into the bloodstream in the non-Cu-bound form for the mutation of the ATP7B gene. In the present study, we analyzed the Cu distribution in the serum of Wilson disease patients by HPLC/inductively coupled plasma-mass spectrometry (ICP-MS). With this method, ceruloplasmin was detected as a Cu peak at a retention time of 12.2 min in the serum of a healthy human. This result demonstrates that holo-ceruloplasmin in human serum was detectable using the present HPLC/ICP-MS method. On the other hand, on Wilson disease patients, no significant Cu was detected within this retention time. These results indicate that a normal level of holo-ceruloplasmin was not detected in the serum of Wilson disease patients. We suggest that the determination of ceruloplasmin by HPLC/ICP-MS in human serum is beneficial as a new tool for the diagnosis of Wilson disease.

抄録全体を表示