Urine and humans

Application to human urine and human serum. The proposed CE-ECL method was applied to the determination of CIP in urinary samples and blood samples. In this study, both urinary samples and blood samples were spiked with different concentrations levels of CIP. Due to the inherent excellent selectivity and sensitivity of the proposed CE-ECL method, the samples were prepared without extra extraction except some simple procedure such as concentration, filtration, and dilution. Fig. 2(A) was the electropherograms of the blank serum sample (a), and 50 Hg/L CIP standard solution was spiked into serum sample as shown in (b). Fig. 2(B)... 

Adachi, J., Mizoi, Y., Naito, T., Ogawa, Y., Uetani, Y. and Ninomiya, I. (1991a) Identification of tetrahydro-beta-carboline-3-carboxylic acid in foodstuffs, human urine and human milk. J. Nutr. 121 646-652. 

Although this procedure tends to eliminate many reineckates which are insoluble under more acidic conditions, the choline content of samples so determined is at best only relative. Further studies have shown that the reineckate obtained from rat liver is contaminated with another component. Acetone solutions so prepared were applied to filter paper strips and developed chromatographically with n-butanol saturated with water they were resolved into two spots, one having an i2/ value of 0.00 and the other 0.7. The Rf value of recrystallized choline reineckate is 0.00 under these conditions. The nature of the faster moving component is unknown. This has been observed in reineckates obtained from methanol extracts of peanut meal, rat urine, and human urine. Washing the precipitate in the funnel, with relatively large amounts (20-30 ml.) of 0.10 N NaOH or 0.1 N HCl saturated Avith choline reineckate and n-propanol, does not remove the contaminant. 

Florfenicol has a wide tissue distribution, similar to that reported for chloramphenicol in calves and thiamphenicol in humans (43,44). Chloramphenicol attains concentrations higher than the corresponding plasma concentrations in bile and urine, as does florfenicol (43). Unlike florfenicol, chloramphenicol concentrations in the Hver, kidney, spleen, and lungs are less than corresponding plasma concentrations. However, chloramphenicol penetrates the brain and CSF much better than does florfenicol, reaching values equal to plasma concentrations in the brain. The distribution of thiamphenicol into the kidney, urine, and muscles of humans compared with corresponding plasma concentration is similar to what was observed for florfenicol in calves (44). The penetration of thiamphenicol into the CSF is much smaller than that of florfenicol in calves. 

The dermal adsorption of DEBT in humans has been studied in the Netherlands by appHcation of DEBT as undiluted technical material or as 15% solutions in alcohol. Labeled material was recovered from the skin, and absorption of DEBT was indicated by the appearance of label in urine after two hours of skin exposure. About 5—8% of the appHed treatments was recovered as metaboHtes from urine, and excretion of metaboHtes in the urine came to an end four hours after exposure ended. DEBT did not accumulate in the skin, and only a small (less than 0.08%) amount ended up in feces. Curiously, less has been absorbed through skin from 100% DEBT appHcation (3—8%, mean of 5.6%) than from 15% alcohol appHcation (4—14%, mean of 8.4%). These results have been described as consistent with previous absorption/metaboHsm studies using guinea pigs, rats, and hairless dogs. Other pubHcations on DEBT toxicology have been cited (92). 

Antibacterial activity of clindamycin is found both in urine and feces after adrninistration of clindamycin. This activity is a consequence of the presence of both clindamycin and its metaboUte, de- /V-methy1c1indamycin [22431-45-4] (6, R = R = H). Unlike de-/V-methy11incomycin, the de-Ai-methyl analogue is as active in vitro as clindamycin. The analogue has been isolated from the urine of humans who had received clindamycin, and its presence in semm has been detected (65). 

Human sensitization studies were negative at 10% solution (47). Undiluted benzyl alcohol produces moderate dermal irritation in guinea pigs and mild dermal irritation in rabbits (48,49). Severe eye irritation was noted in a rabbit study (50). Acute oral rat LD q values were reported between 1.23 and 3.10 g/kg (50—52). A dermal rabbit LD q value of 2.0 g/kg has been reported (49). Rats died after 2 h when exposed to a 200-ppm vapor concentration (53). Benzyl alcohol is readily oxidized in animals and humans to benzoic acid [65-85-0] which is then conjugated with glycine [56-40-6], and rapidly eliminated in the urine as hippuric acid [495-69-2] (54). 

The absorption, distribution, and accumulation of lead in the human body may be represented by a three-part model (6). The first part consists of red blood cells, which move the lead to the other two parts, soft tissue and bone. The blood cells and soft tissue, represented by the liver and kidney, constitute the mobile part of the lead body burden, which can fluctuate depending on the length of exposure to the pollutant. Lead accumulation over a long period of time occurs in the bones, which store up to 95% of the total body burden. However, the lead in soft tissue represents a potentially greater toxicological hazard and is the more important component of the lead body burden. Lead measured in the urine has been found to be a good index of the amount of mobile lead in the body. The majority of lead is eliminated from the body in the urine and feces, with smaller amounts removed by sweat, hair, and nails. 

Quantitation of the oral bronehodilator 2,5-diethyl-7-(tetrahydro-l,4-thiazin-4-yl)-l,2,4-triazolo[l,5-c]pyrimidine (R-836) (195) in plasma and urine of humans and experimental animals utilized reversed-phase HPLC and UV deteetion (88MI1). 

A thin-layer chromatography assay was developed for ffie simultaneous determination of the three major hydroxylated metabolites of antipyrine 409,410, and 411 in urine of humans and other animals (82JPP168) (Scheme 95). 

Alcohol sulfates are easily metabolized by mammals and fishes either by oral or intraperitoneal and intravenous administration. Several labeled 35S and 14C alcohol sulfates have been used to determine their metabolism in experiments with rats [336-340], dogs [339], swines [341], goldfish [342], and humans [339]. From all of these studies it can be concluded that alcohol sulfates are absorbed in the intestine of mammals and readily metabolized by to and p oxidation of the alkyl chain and excreted in the urine and feces, but are also partially exhaled as carbon dioxide. Fishes absorb alcohol sulfates through their gills and metabolize them in a similar way to that of mammals. 

Chiaia AC, Banta-Green C, Field J (2008) Eliminating solid phase extraction with large-volume injection LC/MS/MS analysis of illicit and legal drags and human urine indicators in US wastewaters. Environ Sci Technol 42(23) 8841-8848... 

No studies were located regarding excretion of methyl parathion in humans following inhalation exposure. The limited information available from human case studies indicates that the chemical s metabolites are rapidly excreted primarily in the urine in humans following oral (Morgan et al. 1977) or dermal (Ware et al. 1974, 1975) exposure and in animals following oral (Hollingworth et al. 1973) or dermal (Abu-Qare et al. 2000) exposure. 

Exposure Levels in Humans. Methyl parathion has been detected in serum and tissue shortly after acute exposure (EPA 1978e Ware et al. 1975). It is rapidly metabolized and does not persist in serum and tissues for long (Braeckman et al. 1983). Two metabolites of methyl parathion, 4-nitrophenol and dimethyl phosphate, can be detected in urine and tissues for up to 2 days following exposure (Morgan et al. 1977). These compounds are specific for methyl parathion when there is a history of exposure. 

Methyl parathion was determined in dog and human serum using a benzene extraction procedure followed by GC/FID detection (Braeckman et al. 1980, 1983 DePotter et al. 1978). An alkali flame FID (nitrogen-phosphorus) detector increased the specificity of FID for the organophosphorus pesticides. The detection limit was in the low ppb (pg/L). In a comparison of rat blood and brain tissue samples analyzed by both GC/FPD and GC/FID, Gabica et al. (1971) found that GC/FPD provided better specificity. The minimum detectable level for both techniques was 3.0 ppb, but GC/FPD was more selective. The EPA-recommended method for analysis of low levels (<0.1 ppm) of methyl parathion in tissue, blood, and urine is GC/FPD for phosphorus (EPA 1980d). Methyl parathion is not thermally stable above 120 °C (Keith and Walters 1985). 

Information is available regarding excretion of endosulfan and metabolites in humans. Blanco-Coronado et al. (1992) measured total endosulfan in the urine of poisoned individuals shortly after poisoning occurred. However, it could not be ascertained whether the urine was a major or minor excretion route. a-Endosulfan, P-endosulfan, and/or metabolites were present in the urine of humans after intentional oral exposure (Boerebomm et al. 1998) and after occupational exposure either with (Arrebola et al. 1999) or without (Vidal et al. 1998) protective clothing. 

Exposure Levels in Humans. Endosulfan and endosulfan sulfate can be measured in human blood, urine, and tissues following exposure to high levels in worlq)lace environments or following accidental or intentional ingestion of insechcides containing endosulfan (Coutselinis et al. 1978 Demeter and Heyndrickx 1978 Demeter et al. 1977). However, no monitoring studies are available in which human... 

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