The impact of environmental pollution at the place of residence of pregnant women and of their smoking habits on the cellular energy metabolism of placental tissue was investigated. Samples of full-term placentas were randomly collected from two environmentally different regions of Slovakia (Bratislava, Stará Ľubovňa) and the activity of lactate dehydrogenase (LDH) was measured. Our results showed enhanced LDH activity in the placenta that was dependent on both the type of environmental pollutants at the place of residence and the smoking habits during pregnancy. The enhanced LDH activity may reflect hypoxic conditions due to the accumulation of heavy metals and toxic compounds of tobacco smoke in the placental tissue. A high content of heavy metal particles, found in placental samples from Stará Ľubovňa in our previous studies, might contribute to the increased LDH activity in placentas from this region. We hypothesize that fine metal particles deposited in the placental tissue might be phagocytozed by the syncytiotrophoblast, thus contributing to the decreased oxygen level in placental tissue., A. Kaiglová, E. Reichrtová, A. Adamčáková, L. Wsólová., and Obsahuje bibliografii
Lactate dehydrogenase (LDH) activity and its isoenzymatic fractions were measured in bone marrow blood and in peripheral venous blood from 16 haematologically normal subjects. Total LDH activity was significantly higher in marrow than in venous blood (428.8 ±98.4 vs 260.1 ±40.2 mU/1, p<0.0001). The same was true for the absolute values of its isoenzymatic fractions. The percentage fractions LDH 1 and LDH 5 were similar in the two regions, while LDH 3 and LDH 4 were higher in medullary blood (p<0.05) and LDH 2 was higher in peripheral blood (p<0.05). The Spearman test showed a limited correlation between marrow and peripheral total LDH activity values (p<0.05). This seems to be at least in part sustained by the highly significant correlations existing in LDH 3 and LDH 4 values, reported to be pre-eminent isoforms in maturing haematopoietic cells (p< 0.005 and p< 0.001, respectively). These findings could be attributed to an apoptotic regulation of marrow cell production.
Although there are abundant data on ischemic postconditioning (IPoC) in the adult myocardium, this phenomenon has not yet been investigated in neonatal hearts. To examine possible protective effects of IPoC, rat hearts isolated on days 1, 4, 7 and 10 of po stnatal life were perfused according to Langendorff. Developed force (DF) of contraction was measured by an isometric force transducer. Hearts were exposed to 40 or 60 min of global ischemia followed by reperfusion up to the maximum recovery of DF. IPoC wa s induced by three cycles of 10, 30 or 60 s periods of global ischemia/reperfusion. To further determine the extent of ischemic injury, lactate dehydrogenase (LDH) release was measured in the coronary effluent. Tolerance to ischemia did not change from day 1 to day 4 but decreased to days 7 and 10. None of the postconditioning protocols tested led to significant protection on the day 10. Prolonging the period of sustained ischemia to 60 min on day 10 did not lead to better protection. The 3x30 s protocol wa s then evaluated on days 1, 4 and 7 without any significant effects. There were no significant differences in LDH release between postconditioned and control groups. It can be concluded that neonatal hearts cannot be protected by ischemic postconditioning during first 10 days of postnatal life. and J. Doul, Z. Charvátová, I. Ošťádalová, M. Kohutiar, H. Maxová, B. Ošťádal.