Leukocytes, alkaline phosphatase

Other studies have also shown similar effects on immune functions following acute-duration exposure to benzene. These include decreased numbers of circulating leukocytes and decreases in bone marrow cellularity in mice exposed to 100 ppm and higher, 24 hours per day for up to 8 days (Gill et al. 1980) decreased leukocytes and increased leukocyte alkaline phosphatase in rats exposed to 100 ppm for 7 days (Li et al. 1986) decreased leukocytes and bone marrow cellularity in DBA/2 mice exposed to 300 ppm benzene for 2 weeks (Chertkov et al. 1992) and decreased leukocytes in mice exposed to 300 ppm for 10 days (Ward et al. 1985). These studies are more fully described in Section 2.2.1.2. Decreased spleen weight and levels of B- and T-lymphocytes have also been noted in the blood and spleen of mice exposed 6 hours per day to 47-48 ppm of benzene for 7 or 14 days (Aoyama 1986). Decreased thymus weights were also noted at the 48 ppm dose after 14-day exposure (Aoyama 1986). 

Ward et al. 1985 Wells and Nerland 1991 Wolf et al. 1956 Yin et al. 1982). Both humans (Yin et al. 1982) and rats (Li et al. 1986 Yin et al. 1982) have shown increases in leukocyte alkaline phosphatase activity. No studies regarding effects from oral or dermal exposure in humans were located. However, exposure to benzene through ingestion or dermal contact could cause immunological effects similar to those seen after inhalation exposure in humans and inhalation and oral exposure in animals. 

Li G-L, Yin S-N, Watanabe T, et al. 1986. Benzene-specific increase in leukocyte alkaline phosphatase activity in rats exposed to vapors of various organic solvents. J Toxicol Environ Health 19 581-589. 

Yin S, Li Q, Liang Y. 1982. Significance of leukocyte alkaline phosphatase in the diagnosis of chronic benzene poisoning. Reg Toxicol Pharmacol 2 209-212. 

The transient and moderate rises in leukocyte alkaline phosphatase and uric acid serum concentrations that are often observed after G-CSF treatment are considered to arise from an increased neutrophil count (SEDA-17, 396). Similarly, serum lactate dehydrogenase and alkaline phosphatase activities are often increased, and this should be interpreted as the consequence of enzyme release after growth factor-induced leukocyte recovery (SED-13, 1115). 

A transient, moderate, and reversible rise in leukocyte alkaline phosphatase, lactate dehydrogenase (LDH) and serum uric acid concentrations is usually observed in cancer patients receiving supportive treatment with GM-CSF or G-CSF. Serum LDH increased from 37 to 85% and there was a linear relation between increased leukocyte production and the rise in serum LDH (32). Increases in serum LDH activity should therefore not be interpreted as indicative of disease progression, unless LDH activity remains high after growth factor withdrawal. 

Starch-gel electrophoresis of the alkaline phosphatase in the butanol extracts of leukocytes revealed three variants of the enzyme. Peacock et al. (PI) have devised a method for leukocyte alkaline phosphatase assay. An additional variant was detected in blood leukocytes of leukemia patients treated with 6-mercaptopurine (RIO). Robinson and Pierce (R7) indicated that there might be a fundamental difference in molecular structure of the human serum alkaline phosphatase proteins because serum alkaline phosphatase, when incubated with neuraminidase prior to electrophoresis, demonstrated reduced anodal migration of those isoenzymes that are not L-phenylalanine-sensitive. L-Phenylalanine-sensi-tive enzyme of intestinal origin was found to be neuraminidase-resistant. 

Human leukocytes possess alkaline phosphatase (L13, 03, RIO, T6, V3, V4) whose activity parallels the concentration of certain circulating steroids. Thus, during the menstrual cycle, the leukocyte alkaline phosphatase evidences a peak at midcycle corresponding to the higher estrogen level. In the later stages of pregnancy the enzyme level increases. Corti-coid hormones also exert an effect on leukocyte alkaline phosphatase. 

Polymorphonuclear leukocyte alkaline phosphatase (RIO, T6, V3, V4) has attracted attention with regard to its elevation in mongoloids exhibiting trisomy 21 and its deficiency in patients with chronic myelogenous leukemia in whom one of the short acrocentric chromosomes is missing. Accordingly, there is reason to implicate chromosomes whose genes determine the extent of leukocyte alkaline phosphatase activity. 

A13. Alter, A. A., Lee, S. L., Pourfar, M., and Dobkin, G., Studies of leukocyte alkaline phosphatase in mongolism. A possible chromosome marker. Blood 22, 165-177... 

Przybylowski, J., Pierzchala, W., Panasiewicz, M., Chronic Toxic Actions of Leaded Gasoline 78 Vapors. 3. Blood and Blood Platelet Morphology, Leukocyte Alkaline Phosphatase Activity, and Serum Electrolyte Levels, Biul. Sluzby Sanit. Epidemiol. Wojewodztwa Katowickiego 17 [1973] 61/6 C.A. 81 [1974] No. 146500. 

---