Urine zinc

Urine Zinc. There is a slight fall in the urinary excretion of zinc during dietary deficiency. Difficulties of sample contamination during collection make this of limited practical value. Increases in urine zinc are, however, an important source of loss in the severely injured catabolic patient, although measurement is rarely required except in research studies. 

There is a large increase in urine zinc whenever there is accelerated breakdown of skeletal muscle and other tissue. After injury or in acute starvation the rise in urinary zinc is evidence of a catabolic state (Fell et al., 1973). 

A. Specific levels. There are no specific tests to diagnose or exclude metal fume fever. Blood or urine zinc detenninations do not have a role in clinical diagnosis of the syndrome. 

Atomic absorption using either flame or electrothermal atomization is widely used for the analysis of trace metals in a variety of sample matrices. Using the atomic absorption analysis for zinc as an example, procedures have been developed for its determination in samples as diverse as water and wastewater, air, blood, urine, muscle... 

Dithiocarbamates are chemically characterized by the presence of metals in the molecule (iron, manganese, zinc, etc.) therefore, the measurement of these metals in urine has been proposed as an alternative approach to monitor exposure. For instance, increased urinary excretion of manganese has been reported in workers exposed to mancozeb (Canossa et al., 1993). Available data are at present insufficient to confirm the possibility of using metals as biomarkers of human exposure to DTC. 

The (n)-enantiomer of penicillamine is used clinically in man either as the hydrochloride or as the free amino acid [1], although the (L)-enantiomer also forms chelation complexes. Penicillamine is an effective chelator of copper, mercury, zinc, and lead, and other heavy metals to form stable, soluble complexes that are readily excreted in the urine [2,3]. 

In mammals, cadmium inhibits copper absorption across the intestinal mucosa (Aaseth and Norseth 1986). Intercorrelations of copper with cadmium and zinc in livers of polar bears (Ursus maritimus) are probably mediated by metallothioneins, which may contain all three metals (Braune etal. 1991). In rats, copper protects against nephrotoxicity induced by cadmium, provided that copper is administered 24 h prior to cadmium insult. Specifically, rats given 12.5 mg Cu/kg BW by way of subcutaneous injection 24 h before receiving 0.4 mg Cd/kg BW — when compared to a group receiving Cd alone — did not have excessive calcium in urine and renal cortex or excessive protein in urine. Thus, 2.8 mg Cu/kg BW protects against 0.25 mg Cd/kg BW (Liu et al. 1992). 

Some of the zinc taken up by the intestinal epithelial cells is rapidly transferred to the portal plasma where it associates with albumin, a2 macroglobulin, and amino acids. About 67% of the zinc in plasma is bound to albumin, and about 3% is stored in liver (Stemlieb 1988). Soluble organozinc complexes are passively absorbed across the plasma membrane of the mucosa of the intestinal villi the soluble, nondiffusable complexes are transported in the intestinal products and excreted in feces (NAS 1979). Zinc loss from urine and sweat is usually small (Casey and Hambidge... 

Low-dose kits ate less than other groups. Urine was the most important excretory route in the zinc-deficient group, compared to feces in higher-dose groups (Mejbom 1989). 

Elevated zinc levels in serum, liver, and kidney jaundice, anoxemia, anemia, vomiting, dark red urine. 

Matsumiya etal. 91) determined zinc in both serum and urine by direct dilution. Dawson and Walker92) diluted plasma 20-fold with 0.1 AT hydrochloric acid, in whole blood diluted 100-fold, and in urine diluted 10-fold. Suppression of up to 15 % of the absorbance by inorganic components was overcome by adding the appropriate amounts of those ions to the standards. Willis93) determined zinc in urine by direct aspiration. Other workers have also determined zinc in urine 79>94) and in blood and urine 9S). 

Blood should be deproteinized by some technique which leaves no extra salt, acid, or alkali in the supernatant Some suitable techniques are with tungstic acid, with ethanol (BIO), or with zinc sulphate and barium hydroxide (S21). The supernatant is desalted in the same way as urine and, if necessary, concentrated before applying to the paper. Subsequent technique is as for urine. 

A similar process occurs when we spread a thick paste of zinc and castor oil on a baby s bottom each time we change its nappy. The zinc is in fact zinc oxide, ZnO, which, being amphoteric, reacts with the uric acid in the baby s urine, thereby neutralizing it. 

High levels of dietary zinc were associated with marked decreases in bone calcium deposition and in the apparent retention of calcium in male weanling albino rats. Marked increases in fecal calcium levels were also observed in the zinc-fed rats. Excessive dietary zinc was associated with a shifting of phosphorus excretion from the urine to the feces. This resulted in an increase in fecal phosphorus and provided an environmental condition which would increase the possibility of the formation of insoluble calcium phosphate salts and a subsequent decrease in calcium bioavailability. The adverse effect of high dietary zinc on calcium status in young rats could be alleviated and/or reversed with calcium supplements. 

Table VI shows the effect of 0.75% dietary zinc on the phosphorus balance in young rats. A decrease in the apparent retention of phosphorus was noted in the zinc-fed rats as early as the end of the first week. Possibly a more significant observation was the apparent movement of phosphorus excretion from the urine, the normal pathway for phosphorus excretion, to the feces in rats fed the high zinc diet. Such a shifting of the phosphorus excretion to the fecal pathway in animals fed a high zinc diet should result in an increase...

The data presented in this paper indicate that excess levels (0.75%) of dietary zinc result in decreases in the bioavailability of calcium and phosphorus in rats and interfere with normal bone mineralization. High dietary levels of calcium or zinc appeared to cause a shift in the excretion of phosphorus from the urine to the feces, while the presence of extra phosphorus tended to keep the pathway of phosphorus excretion via the urine. The presence of large amounts of phosphorus in the Intestinal tract due to high intakes of zinc would increase the possibility of the formation of insoluble phosphate salts with various cations, including calcium, which may be present. A shift in phosphorus excretion from the feces to the urine, however, could result in an environmental condition within the system which would tend to increase the bioavailability of cations to the animal. The adverse effect of zinc toxicity on calcium and phosphorus status of young rats could be alleviated with calcium and/or phosphorus supplements. 

Zinc sulfate is claimed to bond with THC metabolites, and because it s a solid, it gets passed as stool rather than urine. Jeff Nightbyrd says it does nothing. Anne Watters Pearson said zinc sulfate is no miracle drug for pissing. Forget it. ... 

---