Rat red cells

Figure 4. Effect of iron intake on the mean corpuscular volume (MCV) of the rat red cell. Diets contained either 10% (O) or 20% (A) protein (5).

Fig. 3. Estimation of frequencies of precursor cells specific for rat red cells (Brown et al., 1966), poly-ala-BSA (Bosma and Weiler, 1970) and EPS (Moller and Michael, 1971) In all three instances, spleen cells from non-immunized mice were used...

Treated rats had 1000 mg/kg FW liver (vs. 4.7 in controls) lowered hemoglobin, hematocrit, and red cell counts mean survival time of 67 days hepatic and renal histopathology Dose-time-dependent increase in copper concentrations in liver, spleen, and lung little accumulation in muscle and skin. Reduced growth at 2.5 and 3.75 mg/kg BW daily reduced survival at 3.75 mg/kg BW. Maximum copper concentrations recorded, in mg/kg FW (vs. saline controls,) were 710 in liver (<5), 212 in kidney (<10), 7 in lung (<1.5), 27 in spleen (<2.0) 6 in bone (<2.0) and 2.2 in testes (<1.6) Increased serum ceruloplasmin and white blood cell number... 

Other workers have determined zinc in serum by direct dilution 87> 88). McPherson and George 89) determined total copper and zinc of red cells and the free copper and zinc of plasma and dialysis fluids of patients undergoing regular hemodialysis, using atomic absorption spectroscopy. Spry and Piper 90) determined zinc in whole blood and plasma in blood cells of iron deficient rats. The zinc concentrations were raised in the iron deficient rats. 

There were no significant changes in red cell counts, hemoglobin concentration, or white cell counts in rats fed doses of 0, 1, 15, or 62 mg/kg/day in the diet for 16 weeks (Gorzinski et al. 1985). 

The Hp concentration in the conventional laboratory animals, rabbit (II, B5), guinea pig, and rat (R3), is considerably lower than in humans, a difference possibly due to the shorter survival of red cells in these species than in humans. 

Hematological Effects. No statistically significant differences in hematological parameters (erythrocyte count, hemoglobin, packed red cell volume) were seen compared to controls in hybrid rats (10 of each sex) exposed to up to 11.6 mg/m3 diazinon (nose-only) for 3 weeks, 5 days a week for 6 hours a day (Hartman 1990). 

Methoxy-8-hydroxylaminoquinoline, an N-hydroxylated metabolite of primaquine (Fig. 7.46), is directly toxic, causing hemolysis and methemoglobinemia in rats. However, there are several pathways of metabolism for primaquine and several potential toxic metabolites. Thus, hydroxylation of primaquine at the 5-position of the quinoline ring also forms redox-active derivatives able to cause oxidative stress within normal and G6PD-deficient human red cells as well as rat erythrocytes (Fig. 7.46). 

The hemolytic activity in vivo has not been directly linked to these metabolites. However, recent research has used a combination of in vitro and in vivo studies in which isolated red cells were exposed to a particular metabolite, then the cells were put back into the rats from whence they came, and their survival monitored. This research has confirmed the role of these two reactive metabolites as involved in the toxicity. 

Rats and dogs given intravenous doses of triethylene glycol diglycidyl ether showed necrosis of the renal tubule epithelium, of the adrenal cortex and of the intestinal epithelium. In dogs, blood neutrophils disappeared and lymphocyte counts fell to 50% of normal. Though the erythrocyte and platelet counts remained constant, the brief appearance of polychromatic and nucleated red cells indicated that erythropoiesis was also affected. 

Monis, B., Rovasio, R. A. and Valentich, M. A. 1975. Ultrastructural characterization by ruthenium red of the surface of the fat globule membrane of human and rat milk with data on carbohydrates of fractions of rat milk. Cell Tiss. Res. 157, 17-24. 

In 1924, Martland et al. (1) reported on phosphatase activity in red blood cells. Roche later differentiated between the phosphatase of the red cells with pH optimum 6.0-6.2 and the phosphatase from white cells with optimum 8.8-9.0. Roche also showed that a-glycerophosphate was split more rapidly than -glycerophosphate by red cell extracts while the reverse was true of acid phosphatase activity in plasma (2). While studying the source of acid phosphatase activity in male urine, Kutscher and Wolberg discovered the very high activity of acid phosphatase in human prostate (3). This tissue was shown by Woodard to have one-thousand times the activity of extracts from bone, liver, and kidney (3a). Igarashi and Hollander crystallized the acid phosphatase of rat liver and showed that under certain conditions allosteric control of the activity could be demonstrated (4). 

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