Enhanced Fetal Erythrocyte Carbonic Anhydrase Activity by Hydrocortisone

Abstract

Pediat. Res. 10: 779-782 (1976) Carbonic anhydrase hyaline m e m b r a n e disease ExtractThe present experiments were undertaken to study the effect of exogenous corticosteroids on carbonic anhydrase ( C A ) activity in fetal erythrocytes. Rabbit fetuses from 24 days of gestation to term (31 days) were injected intraperitoneally with either 0.2 ml of 0.9% saline or 2.5 mg hydrocortisone succinate. Nonoperated, noninjected animals served as controls. Carbonic anhydrase activity measured at 24 hr after injection was increased in the saline-injected group at all ages studied when compared with the noninjected fetuses. A marked increase (2-to 7-fold) in enzyme activity was demonstrated after steroid injection at 24 but not 48 hr after treatment. An increase in CA activity was also demonstrated after incubating fetal erythrocytes for 2, 4, and 8 hr in the presence of hydrocortisone succinate. It is suggested that low CA activity in infants with hyaline membrane disease ( H M D ) may reflect lack of enhancement by steroid. SpeculationGlucocorticoids are probably important in the enhancement of the development of numerous organ systems, including lung, gut, and blood, in preparation for extrauterine life. Low CA activity in the cord blood of infants with H M D may reflect a lack of steroid activation of a number of fetal enzyme systems, including those necessary for surfactant synthesis.Carbonic anhydrase is an enzyme that reversibly catalyzes the hydration of carbon dioxide to bicarbonate and hydrogen ions. Early investigations have determined that CA activity is lower in the fetus than in the newborn and that both have values lower than the adult (I, 3, 6, 18). More recently, investigators from the United States have demonstrated that the CA activity in the cord blood of infants with HMD is markedly lower than in infants of the same gestational age without HMD (7,8,16), although the reason for this remains unknown. However, Logan et a/. (10) studied infants with and without HMD and measured CA activity in erythrocytes obtained within the first 24 hr of birth. They found no difference in CA activity. Several investigators have shown an acceleration of fetal lung maturation by the in vivo administration of corticosteroids (4, 5, 9, l I, 15, 20). With this in mind, the present study was undertaken to determine whether steroids could also enhance carbonic anhydrase activity in the fetus, and whether this might explain the discrepant results reported for CA activity in infants with HMD. M E T H O D SForty-two pregnant New Zealand albino rabbits from 24 to 30 days of gestation were used for this study. The does were mated with two bucks within a 2-hour period and this time was considered to be day 0 of gestation. The rabbits were then removed and kept in separate cages for the duration of the experiment. On the appropriate day, a laparotomy was performed on the adults through a.midline incision. The fetal abdomen was identified by palpation and an injection of either 0.2 ml 0.9% saline or 2.5 mg hydrocortisone succina...

Cortisol alters carbonic anhydrase-mediated renal sulfate secretion

“…As noted above, cortisol has been shown to stimulate CA activity in the mammalian brain (13) and red blood cell (39). Reducing cortisol to low physiological levels reduced CA activity 28% and CAII protein abundance 65% in fPTC cell lysates.…”

“…Sexual maturation induces an increase in CA activity in red blood cells and kidneys of rabbits (6), and dexamethasone (a cortisol agonist) treatment (in vivo) of rats accelerates the maturation-induced increase in CA activity in the brain (13). CA activity in red blood cells is increased by in vitro and in vivo cortisol treatment (39). SO 4 2Ϫ secretion, reabsorption, and urinary acidification are all affected, directly or indirectly, by glucocor-ticoids (3,12,36), respectively.…”

Activity of Carbonic Anhydrase in Stored Blood

“…Carbonic anhydrase concentrations are much smaller in the red cells of the newborn (Mondrup and Anker, 1975) and are increased in a number of pathological states (Mondrup and Anker, 1976). It has been found that thyroid hormones (Kondo et al, 1978) and hydrocortisone (Russell, Loesebrink and Chernick, 1976) affect the amount of enzyme in the red cells. The activity of the normal enzyme is altered in the presence of phosphate compounds (Narumi and Miyamoto, 1974) and various anions (Maren, Rayburn and Liddell, 1976).…”

Effect of NaHS on carbonic anhydrase activity of human erythrocyte

“…Alteration of this enzyme activity has been reported by the effect of advanced glycation end products, methylglyoxal and reduced glutathione. [10][11][12] Recently research proved that CA inhibition represents an effective therapeutic approach towards mitigation of hypertrophic cardiac myocyte growth. 13 CAs also act on medullary chemoreceptors at two sites.…”

“…Outside the blood -brain -barrier it acts as plasma buffer, whereas inside the barrier it accelerates CO 2 /pH equilibrium. 14 The enzyme also has definite role in neuromuscular transmission. 15 So in recent years, study of carbonic anhydrases, one of the fastest enzymes of biological system, draw attention in medical research not only for its physio-biochemical action, but also for its association with different pathological processes as discussed above.…”