Quantitative and qualitative analysis of lipids has been performed on a rhoptry fraction purified from Toxoplasma gondii tachyzoites. The lipid to protein ratio was estimated to be 0.26. The cholesterol to phospholipid ratio was unusually high at 1.48. Phosphatidylcholine was the major phospholipid; phosphatidylserine, phosphatidylinositol and sphingomyelin were absent whereas significant amounts of phosphatidic acid and lysophospholipids were found. This pelicular composition could be related to functional involvement of the organelle in host-cell invasion.

The present investigation was undertaken to evaluate whether mitochondrial energy metabolism is altered in a model of malnutrition induced by dexamethasone (DEX) treatment (1·5 mg/kg per d for 5 d). The gastrocnemius and liver mitochondria were isolated from DEX-treated, pair-fed (PF) and control (CON) rats. Body weight was reduced significantly more in the DEX-treated group (2 16 %) than in the PF group (2 9 %). DEX treatment increased liver mass (þ 59 % v. PF, þ23 % v. CON) and decreased gastrocnemius mass. Moreover, in DEX-treated rats, liver mitochondria had an increased rate of non-phosphorylative O 2 consumption with all substrates (approximately þ42 %). There was no difference in enzymatic complex activities in liver mitochondria between rat groups. Collectively, these results suggest an increased proton leak and/or redox slipping in the liver mitochondria of DEX-treated rats. In addition, DEX decreased the thermodynamic coupling and efficiency of oxidative phosphorylation. We therefore suggest that this increase in the proton leak and/or redox slip in the liver is responsible for the decrease in the thermodynamic efficiency of energy conversion. In contrast, none of the variables of energy metabolism determined in gastrocnemius mitochondria was altered by DEX treatment. Therefore, it appears that DEX specifically affects mitochondrial energy metabolism in the liver. Glucocorticoid: Mitochondrion: Oxidative phosphorylation: Respiratory chain complexesMalnutrition is prevalent in many patients, especially in those who are elderly. It causes increased mortality, significant hospital expenditure, reduced muscle and immune function, and decreased quality of life (Wallace et al. 1995;Tucker & Miguel, 1996;Chima et al. 1997;Lesourd & Mazzari, 1997;Landi et al. 2000). Malnutrition results from a negative energy balance, a situation where energy intake fails to meet energy requirements. Although anorexia and a reduced energy intake are always associated with malnutrition, in some clinical circumstances, an increased resting O 2 consumption rate (referred to as increased energy requirements) can be shown (Nguyen et al. 1999). In contrast, most studies with human subjects and animals show that energy restriction decreases energy expenditure (Ramsey et al. 2000). Therefore, it appears that in these clinical states, adaptive mechanisms that lead to a reduction of energy requirements fail to operate. However, the biochemical nature of this negative energy balance phenomenon, i.e. the increased energy expenditure, is poorly understood at the present time. A wasting of energy may be a possible explanation. In other words, the mitochondrial oxidative phosphorylation yield may be less efficient, and in turn O 2 consumption may be increased, for a same ATP synthesis rate.High-dose glucocorticoid treatment affects body weight and body composition (Kochakian & Robertson, 1951;Hausberger & Hausberger, 1958). It has also been found to induce a hypercatabolic state that leads to a reduced muscle mass (Marone et al. 1994;Minet-Q...

We investigated the role that mitochondrial proton leak may play in the glucocorticoid-induced hypermetabolic state. Sprague^Dawley rats were injected with dexamethasone over a period of 5 days. Liver mitochondria and gastrocnemius subsarcolemmal and intermyo¢brillar mitochondria were isolated from dexamethasone-treated, pair-fed and control rats. Respiration and membrane potential were measured simultaneously using electrodes sensitive to oxygen and to the potential-dependent probe triphenylmethylphosphonium, respectively. Five days of dexamethasone injection resulted in a marked increase in the basal proton conductance of liver mitochondria, but not in the muscle mitochondrial populations. This e¡ect would have a modest impact on energy expenditure in rats.

No abstract

A new diterpene, (4S,9R,10R) methyl 18-carboxy-labda-8,13(E)-diene-15-oate has been obtained from the stem barks of Polyalthia macropoda (Annonaceae). This labdanic derivative was identified on the basis of spectroscopic data and is biologically active against the promastigote Leishmania donovani donovani.