Monkey erythrocytes

A 30-min LC50 of 250 mg/m3 for monkeys was reported by RTECS (1987). Effects included hemolysis without anemia and abnormal erythrocytes. 

In a study by Kensler et al. (1946), three monkeys were exposed by inhalation to arsine at a concentration of 0.45 mg/L (450 mg/m3 or 140 ppm) for 15 min. Although one monkey died in 24 h, one remaining monkey survived without treatment another was treated with 2,3-dimercaptopropyl ethyl ether. The surviving monkey that was not treated could "scarcely raise himself from the floor of his cage from the 2nd to the 7th days." The erythrocyte count of this monkey decreased to 65% of pre-treatment level in 24 h, and by d 3 1 decreased to approximately 20% prior to recovery. The monkey treated with... 

Figure 2. Atomic force microscopy images showing the surface of a rhesus monkey erythrocyte membrane. Damage, such as formation of humps on the peripheral surface and pits in other parts, results from the interaction with virions of the canine parvovirus, (a) edge of erythrocyte (b) pits on membrane surface. (Source http //www.ntmdt.ru/ publications/download/211.pdf, Reproduced with permission from Dr Boris N. Zaitser)...

In the Rh system (not shown), proteins on the surface of the erythrocytes act as antigens. These are known as rhesus factors, as the system was first discovered in rhesus monkeys. 

Cossum PA, Rickert DE. 1987. Metabolism and toxicity of dinitrobenzene isomers in erythrocytes from Fischer-344 rats, rhesus monkeys and humans. Toxicol Lett 37 157-163. 

Decreased PCV and serum protein developed in monkeys exposed to FireMaster FF-1 in dosages of >0.73 mg/kg/day for >25 weeks (two animals) additional hematologic effects observed in one monkey exposed to 18 mg/kg/day for 137 days were decreased erythrocyte and white blood cell counts (Allen et al. 1978 Lambrecht et al. 1978). No hematological changes were measured in cows treated with... 

There are several relatively new therapeutic modalities for the treatment of SLE. Trying to eliminate pathogenic anti-dsDNAs, Ferguson etal. developed an antigen-based heteropolymer (AHP) (F3). AHP is a bispecific dsDNA x monoclonal antibody (mAb) complex (dsDNA x anti-CRl mAb) that enables the use of the unique immune complex-binding and clearing capacity of the complement receptor (CR1) on primate erythrocytes. In vitro studies of AHP show a substantial reduction (>90%) of anti-dsDNA titer (F20). In vivo studies in two rhesus monkeys indicate that the erythrocyte-bound antibodies are rapidly cleared from the circulation (F3). 

Woodard, C.L., Calamaio, C.A., Daminskis, A., Anderson, D.R., Harris, L.W., Martin, D.G. (1994). Erythrocyte and plasma cholinesterase activity in male and female rhesus monkeys before and after exposure to sarin. Fundam. Appl. Toxicol. 23 342-7. 

The continuous cultivation of P. faloiparum in human erythrocytes has been recently accomplished by Trager and Jensen.34 The parasite, originally derived from an infected Aotus trivirgatus monkey, propagated over 100 million times by the addition of human erythrocytes at 3 to 4-day intervals. 

Hematological effects of 2-butoxyethanol have been observed in animals after acute and intermediate inhalation exposure. One male monkey and one female monkey exposed to 200 ppm 2-butoxyethanol for 7 hours did not show any alteration of erythrocyte fragility or evidence of hemoglobinuria (Carpenter et al. 1956). However, one rhesus monkey exposed to 210 ppm 2-butoxyethanol for up to 30 days exhibited elevated osmotic fragility after the fourth exposure, increased fibrinogen after the 14th day, and reduced... 

In this chapter, our intent is to review the rapid changes that take place in the cerebral cortex of n-3 fatty acid-deficient monkeys when their diet is subsequently supplied with ample dietary n-3 fatty acids. Juvenile rhesus monkeys who had developed n-3 fatty acids deficiency since intrauterine life were repleted with a fish-oil diet rich in n-3 fatty acids, DHA, and 20 5n-3 (eicosapentaenoic acid, EPA). The fatty acid composition was determined for the lipid classes of plasma and erythrocytes and for the phospholipid classes and molecular species of frontal cortex samples obtained from serial biopsies and at the time of autopsy. From these analyses, the half-lives ofDHA and EPA in the phospholipids of plasma, erythrocytes, and cerebral cortex were estimated. The deficient brain rapidly regained a normal or even supernormal content ofDHA with a reciprocal decline in n-6 fatty acids, demonstrating that the fatty acids of the gray matter of the brain turn over with relative rapidity under the circumstances of these experiments. 

Fig. 2. The time-course of mean fatty acid changes in erythrocyte phospholipids after tire feeding of fish oil. Note that reciprocal changes of the two major n-3 (EPA and DHA) and the two major n-6 (18 2 and 20 4) polyunsaturated fatty acids occuned as n-3 fatty acids increased and n-6 fatty acids decreased. The concentrations of these four fatty acids in the erythrocyte phospholipids of monkeys fed the control soybean-oil and the deficient safflower-oil diet from our previous study (Neuringer et al, 1986) are given for comparison. Expressed as percentage of total fatty acids, DHA in control monkeys was 1.7 0.9% EPA, 0.5 0.1% 20 4 n-6,15.4 0.5% 18 2 n-6,25.7 1.0%. In deficient monkeys,DHA was0.2 0% EPA was 0% 20 4n-6,18 2 1.3 18 2 n-6 was 25.2 0.4%.

Using the serial data for the cerebral cortex, plasma, and erythrocytes, we constructed accumulation and decay curves for several key fatty acids in these tissues, which provided gross estimates of their turnover times after fish-oil feeding to n-3 fatty acid-deficient monkeys (Table 2). For cerebral cortex, a steady state was reached after 12 wk of fish-oil feeding for DHA, but 22 5n-6 took longer to decline to the low levels found in the cortex of control animals. The half-lives of DHA in cerebral phospholipids ranged from 17 to 21 d 21 d for phosphatidylethanolamine, 21 d for phosphatidylserine, 18 d for phosphatidylinositol, and 17 d for phosphatidylcholine. The corresponding values for 22 5n-6 in these same phospholipids were 32,49,14, and 28 d, respectively. The half-lives of linoleic acid, EPA, and DHA in plasma phospholipids were estimated to be 8,18, and 29 d, respectively. In the phospholipids of erythrocytes, linoleic acid, arachidonic acids, EPA, and DHA had half-lives of 28, 32, 14, and 21 d, respectively. 

Connor WE, Neuringer MA, Lin DS. Dietary effects on brain fatty acid composition the reversibility of n-3 fatty acid deficiency and turnover of docosahexaenoic acid in the brain, erythrocytes, and plasma of rhesus monkeys. J Lipid Res 1990 31 237-247. 

---