Relationship between Growth and Ageing in <Emphasis Type="Italic">Drosophila</Emphasis>

THERE are two principal groups of theories of ageing—those which hold that random cell damage is chiefly responsible for the events characteristic of ageing, which culminate in death and those which hold that ageing and death are genetically controlled. It is too soon to decide between these points of view and in any case Bullough¹ has shown that they are not mutually exclusive. So far experiments to test the random error theories of ageing, involving exposure of organisms to unnaturally large or even small amounts of agents such as X-rays and mutagenic agents (for reviews, see refs. 2 and 3), have been controversial and inconclusive.     

Venography in the evaluation of the results of surgical treatment of varicocele in children]

The paper is concerned with analysis of the results of intraoperative phlebotesticulography, performed in 50 patients with varicocele of degree I-II during Ivanissevich's operation. The effect of surgical intervention was shown to depend upon the quality of ligation of the testicular vein, some parts of which are anastomosed between themselves. The localization of this anastomosis is revealed by means of intraoperative phlebotesticulography, which permits increasing the results of surgical treatment and predicting a course of a postoperative period.     

Toxicity of Dopamine to Striatal Neurons In Vitro and Potentiation of Cell Death by a Mitochondrial Inhibitor

Abstract: Intrastriatal injections of the mitochondrial toxins malonate and 3-nitropropionic acid produce selective cell death similar to that seen in transient ischemia and Huntington's disease. The extent of cell death can be attenuated by pharmacological or surgical blockade of cortical glutamatergic input. It is not known, however, if dopamine contributes to toxicity caused by inhibition of mitochondrial function. Exposure of primary striatal cultures to dopamine resulted in dose-dependent death of neurons. Addition of medium supplement containing free radical scavengers and antioxidants decreased neuronal loss. At high concentrations of the amine, cell death was predominantly apoptotic. Methyl malonate was used to inhibit activity of the mitochondrial respiratory chain. Neither methyl malonate (50 µ M ) nor dopamine (2.5 µ M ) caused significant toxicity when added individually to cultures, whereas simultaneous addition of both compounds killed 60% of neurons. Addition of antioxidants and free radical scavengers to the incubation medium prevented this cell death. Dopamine (up to 250 µ M ) did not alter the ATP/ADP ratio after a 6-h incubation. Methyl malonate, at 500 µ M , reduced the ATP/ADP ratio by ∼30% after 6 h; this decrease was not augmented by coincubation with 25 µ M dopamine. Our results suggest that dopamine causes primarily apoptotic death of striatal neurons in culture without damaging cells by an early adverse action on oxidative phosphorylation. However, when combined with minimal inhibition of mitochondrial function, dopamine neurotoxicity is markedly enhanced.     

Why do antioxidants fail to provide clinical benefit?

The results of recent randomized trials to test the influence of antioxidants on coronary-event rates and prognosis in patients with coronary-artery disease were disappointing. In none of these studies did the use of vitamin E improve prognosis. In contrast, treatment of coronary-artery disease with angiotensin-converting-enzyme (ACE) inhibitors reduced coronary-event rates and improved prognosis. ACE inhibition prevents the formation of angiotensin II, which has been shown to be a potent stimulus of superoxide-producing enzymes in atherosclerosis. The findings suggest that inhibition of superoxide production at enzymatic levels, rather than symptomatic superoxide scavenging, may be the better choice of treatment.     

Sex-related dimorphism of the morphofunctional characteristics of the epiphysis in newborn children subjected to hypoxic impairment and asphyxia

In 72 newborn children (37 boys and 35 girls) who suffered from prenatal hypoxia and were born in an asphyxic state, we measured the level of melatonin in the umbilicial blood and observed clinical manifestations of the adaptation/stress syndrome. These data were compared with the results of morphological examination of the epiphyses from 27 stillborns (15 boys and 12 girls) who perished because of heavy prenatal hypoxia. The level of melatonin in the blood of ill newborn girls was much higher than that in boys, and both these indices were about two times higher than those in respective groups of healthy newborn children. At the same time, the pathomorphological examination showed that active epiphyseal cell units in the male fetuses were much more numerous. The results show that the epiphysis plays a significant role in determination of the sex-related dimorphism of the adaptation/stress syndrome in newborn children suffering from hypoxia- and asphyxia-evoked heavy CNS damage. The reasons and consequences of more intensive morphofunctional loading of the epiphyseal system in the male fetuses are discussed.