Biliary and Urinary Excretion of Metals in Humans

Ishihara, Nobuo; Matsushiro, Takashi

doi:10.1080/00039896.1986.9936705

Cited by 45 publications

(11 citation statements)

References 29 publications

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“…The rate of urinary excretion following the intravenous administration of cobalt chloride was very rapid and the majority of the dose was eliminated by 12 h. The total fecal elimination was approximately 10% of the dose, and supported the finding that cobalt can be secreted in the bile in animals and in humans (Ulrich & Copp, 1950;Stelzer & Klaassen, 1985;Ishihara & Matsushiro, 1986). Gregus and Klaassen (1986) found that cobalt secreted in the bile was not reabsorbed by the small intestine.…”

supporting

confidence: 64%

Disposition, Toxicity, and Intestinal Absorption of Cobaltous Chloride in Male Fischer 344 Rats

Ayala-Fierro¹,

Firriolo²,

Carter³

1999

Journal of Toxicology and Environmental Health

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The absorption and disposition of inorganic cobalt salts after oral administration have not been well characterized. The objectives of this study were to compare in vivo results with cobalt transport through the in vitro everted small intestine and to relate the disposition results to a biochemical indicator of cobalt toxicity. Cobalt chloride was given to male Fischer 344 rats orally at 33.3 mg Co(II)/kg or intravenously at 4.16 mg Co(II)/kg. By 36 h, 74.5% of the oral dose was eliminated in the feces. The liver, kidney, and heart accumulated cobalt to the greatest extent. Following the single oral dose, the blood cobalt concentration-time curve was triphasic, peaked at 3.2 h, and had an absorptive half-life of 0.9 h, an elimination phase half-life of 3.9 h, and a terminal elimination half-life of 22.9 h. Following intravenous administration, 10.1% of the dose was excreted in the feces, indicating that cobalt can be secreted in the bile. Following a single intravenous injection, the concentration-time curve displayed three segments. The first segment, which occurred during the first 4 h, had a rapid half-life of 1.3 h. The second phase, from 4 to 12 h, demonstrated a slower clearance rate with a half-life of 4.3 h. The final and slowest phase, from 12 to 36 h, had a half-life of 19 h. Intestinal jejunal ring experiments indicated that cobalt transport has both active and passive components; however, cobalt transport through the in vitro rat everted duodenum indicated that cobalt transport had almost exclusively passive components with facilitated diffusion. The finding that uptake was saturable may explain the small extent of absorption following oral dosing. Heme oxygenase studies following subcutaneous and intravenous administration resulted in an increase in activity (twofold) over controls, while oral administration did not. We concluded that the extent of cobalt absorption across the gastrointestinal tract is incomplete, and that the concentration administered and the route of exposure may determine its systemic toxicity.

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supporting

confidence: 64%

Disposition, Toxicity, and Intestinal Absorption of Cobaltous Chloride in Male Fischer 344 Rats

Ayala-Fierro¹,

Firriolo²,

Carter³

1999

Journal of Toxicology and Environmental Health

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“…From the results presented it appears that Cu homeostasis is maintained through control of only endogenous excretion and not absorption. Although the present study does not include data on urinary output, it has been reported that this form of excretion is minimal (Ishihara & Matsushiro, 1986) and is not dependent on dietary Cu intake. Turnlund et al (1989Turnlund et al ( , 1998 have performed two dietary intervention studies with male volunteers, feeding Cu levels similar to those used in the present study.…”

Section: Discussionmentioning

confidence: 91%

Adaptive responses in men fed low- and high-copper diets

et al. 2003

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The study of Cu metabolism is hampered by a lack of sensitive and specific biomarkers of status and suitable isotopic labels, but limited information suggests that Cu homeostasis is maintained through changes in absorption and endogenous loss. The aim of the present study was to employ stable-isotope techniques to measure Cu absorption and endogenous losses in adult men adapted to low, moderate and high Cu-supplemented diets. Twelve healthy men, aged 20 -59 years, were given diets containing 0·7, 1·6 and 6·0 mg Cu/d for 8 weeks, with at least 4 weeks intervening washout periods. After 6 weeks adaptation, apparent and true absorption of Cu were determined by measuring luminal loss and endogenous excretion of Cu following oral administration of 3 mg highly enriched 65 Cu stable-isotope label. Apparent and true absorption (41 and 48 % respectively) on the low-Cu diet were not significantly different from the high-Cu diet (45 and 48 % respectively). Endogenous losses were significantly reduced on the low-(0·45 mg/d; P,0·001) and medium-(0·81 mg/d; P¼0·001) compared with the high-Cu diet (2·46 mg/d). No biochemical changes resulting from the dietary intervention were observed. Cu homeostasis was maintained over a wide range of intake and more rapidly at the lower intake, mainly through changes in endogenous excretion.

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“…Cd excret includes Cd from either of two sources, namely, Cd in the bile, 14) which originates both in Cd currently absorbed and Cd moved from the organs storing Cd, such as the liver and kidneys, and Cd from peeled epithelial cells and other intrinsic sources (Fig. 1).…”

Section: Definition Of CD Uptake and Cd Intake-output Balancementioning

confidence: 99%

“…Itai-Itai disease is one disastrous example of chronic Cd poisoning. Food is the main source of Cd intake for non-occupationally exposed people, and the average dietary Cd intake by the Japanese general population was recently calculated as 28 µg/d 1) , much higher than that in other countries; e.g., 9.9 in China 2) , 7.3 in Malaysia 3) , 14.5 in Finland 4) , 8.3 in Sweden 5) and 9 to 10 in Germany 6) . In Japan, rice and shellfish are the major sources of Cd intake, and other foods sold in Japanese markets contain a very wide range of Cd concentrations 7) .…”

mentioning

confidence: 99%

Uptake of Cadmium in Meals from the Digestive Tract of Young Non‐smoking Japanese Female Volunteers

Kikuchi

Nomiyama

Kumagai

et al. 2003

Journal of Occupational Health

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as (1-Cd-F excess /Cd-I excess ) ( Fig. 1), was 47.2% (range: -9.4-83.3%) in Group D1 and 36.6% (range: -9.2-73.5%) in Group D3, and the Cd balance rate, defined as (1-Cd-F output /Cd-I intake ), was 23.9% (range: -4.0-37.7%) in Group D1 and 23.7% (range: -8.2-56.9%) in Group D3. Conclusions-Cd-F and Cd-B are better biological monitoring parameters for assessing change in Cd-I than Cd-U. The Cd uptake and Cd balance rates appeared to be higher than those in previous papers when ingested Cd mainly originated in rice. (J Occup Health 2003; 45: 43-52) Key words: Cadmium, Volunteer experiment, Rice, Dietary intake, Absorption, Biological monitoring Toxicity due to cadmium (Cd) accumulation in the body is known to cause renal damage and resultant osteoporosis. Itai-Itai disease is one disastrous example of chronic Cd poisoning. Food is the main source of Cd intake for non-occupationally exposed people, and the average dietary Cd intake by the Japanese general population was recently calculated as 28 µg/d 1) , much higher than that in other countries; e.g., 9.9 in China 2) , 7.3 in Malaysia , 8.3 in Sweden 5) and 9 to 10 in Germany 6) . In Japan, rice and shellfish are the major sources of Cd intake, and other foods sold in Japanese markets contain a very wide range of Cd concentrations 7) . In order to determine a tolerable level of Cd intake from meals, we must establish a non-observed adverse effect level (NOAEL) based on the dose-response relationship between Cd in foods and adverse effects on the kidneys. At present, however, such data are not available, and in fact, a large-scale prospective study to establish the NOAEL is currently considered infeasible.On the other hand, the dose-response relationships

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Biliary and Urinary Excretion of Metals in Humans

Cited by 45 publications

References 29 publications

Disposition, Toxicity, and Intestinal Absorption of Cobaltous Chloride in Male Fischer 344 Rats

Disposition, Toxicity, and Intestinal Absorption of Cobaltous Chloride in Male Fischer 344 Rats

Adaptive responses in men fed low- and high-copper diets

Uptake of Cadmium in Meals from the Digestive Tract of Young Non‐smoking Japanese Female Volunteers

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