Blood urinary control

Hamano, K, et al (2002). Blood sugar control reverses the increase in urinary... 

Inhibition of ALAD and stimulation of ALAS result in increased levels of ALA in blood or plasma and in urine. For example, in a case report of a 53-year-old man with an 11-year exposure to lead from removing old lead-based paint from a bridge, a PbB level of 55 pg/dL was associated with elevated urinary ALA (Pollock and Ibels 1986). The results of the Meredith et al. (1978) study on lead workers and controls indicated an exponential relationship between PbB and blood ALA. Numerous studies reported direct correlations between PbB level and log urinary ALA in workers. Some of these studies indicated that correlations can be seen at PbB levels of <40 pg/dL (Lauwerys et al. 1974 Selander and Cramer 1970 Solliway et al. 1996), although the slope may be different (less steep) than at PbB levels of >40 pg/dL. In a study of 98 occupationally exposed subjects (51 pg/dL, mean PbB) and 85 matched controls (20.9 pg/dL. mean PbB) it was found that log ZPP and log ALA in urine correlated well with PbB levels (Gennart et al. 1992a). In the exposed group, the mean ZPP was 4 times higher than in the controls, whereas urinary ALA was increased 2-fold. 

Blood lead levels, urinary lead levels, serum creatinine, blood urea nitrogen (BUN), creatinine clearance (CCT), and NAG were measured in 158 male and 51 female workers in a lead battery factory or a lead smelting plant in Japan (Ong et al. 1987). Controls consisted of 30 professional and laboratory staff members with no history of renal disease or lead exposure. The length of exposure to lead averaged 10.8 8.0 years with a range of 1-36 years. Exposure levels were not available, but indicators of lead body burden in the exposed workers were PbB level = 3.0-80.0 pg/dL and urinary lead level =... 

Moreover, several buffer systems exist in the body, such as proteins, phosphates, and bicarbonates. Proteins are the most important buffers in the body. Protein molecules contain multiple acidic and basic groups that make protein solution a buffer that covers a wide pH range. Phosphate buffers (HPO T /H2P07) are mainly intracellular. The pK of this system is 6.8 so that it is moderately efficient at a physiological pH of 7.4. The concentration of phosphate is low in the extracellular fluid but the phosphate buffer system is an important urinary buffer. Bicarbonate (H2C03/HC0 3) is also involved in pH control but it is not an important buffer system because normal blood pH 7.4 is too far from its pK 6.1 [144],... 

None of the exposures produced changes in clinical chemistry values (blood count, blood nitrate, blood urea nitrogen, serum enzymes, and serum electrolytes or urinalysis and nitrate and nitrite urinary excretion), spontaneous electrical activity of the cortex of the brain (detected by EEG), pulse rate and sinus rhythm, or pulmonary function. Visual and auditory acuity, exercise EKG, and time estimation tests did not differ from control values for any of the exposures. Only one of several cognitive tests was affected by exposure and the change occurred only in the four subjects exposed at 1.5 ppm. The test was taken during the time the subjects were experiencing severe headaches. 

Levels of cyanide and its metabolite thiocyanate in blood serum and plasma, urine, and saliva have been used as indicators of cyanide exposure in humans, particularly in workers at risk of occupational exposures, in smokers or nonsmokers exposed to sidestream or environmental tobacco smoke, in populations exposed to high dietary levels of cyanide, and in other populations with potentially high exposures (see Section 5.6). The correlation between increased cyanide exposure and urinary thiocyanate levels was demonstrated in workers exposed to 6.4-10.3 ppm cyanide in air (El Ghawabi et al. 1975). In another study, blood cyanide concentrations were found to vary from 0.54 to 28.4 pg/100 mL in workers exposed to approximately 0.2-0.8 ppm cyanide in air, and from 0.0 to 14.0 pg/100 mL in control workers... 

In one study we explored sixty items in a small group of alcoholics and nonalcoholic controls in the hopes of finding some metabolic peculiarities which might be associated with alcoholism-proneness.2 These sixty items included urinary constituents, salivary constituents, and blood constituents. There were six items which appeared to be significantly different for the two groups. Subsequently, more extensive investigations have indicated that certain of these items are, with even higher probability, distinctively different for alcoholics.3... 

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