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Les fruits et légumes issus de pratiques écologiques se distinguent mal des produits courants de l’agriculture intensive, lorsqu’on les compare à l’aide des critères classiques d’analyses sur les nutriments, vitamines et oligoéléments.

Induction of β‐methylcrotonyl‐coenzyme A carboxylase (MCCase) activity was observed during carbohydrate starvation in sycamore cells. In mitochondria isolated from starved cells, we noticed a marked accumulation of the biotinylated subunit of MCCase, of which the apparent molecular weight of 74 000 was similar to that of the polypeptide from mitochondria of potato tubers. Our results provide evidence for a role of MCCase in the catabolic pathway of leucine, a branched‐chain amino acid which transiently accumulates in carbon‐starved cells in relation to a massive breakdown of proteins. Furthermore, when control sycamore cells were incubated in the presence of exogenous leucine, this amino acid accumulated in the cells and no induction or accumulation of MCCase was observed, indicating that leucine is not responsible for the induction of its catabolic machinery. Finally, MCCase is proposed as a new biochemical marker of the autophagic process triggered by carbohydrate starvation.

This review examines the parameters of enzymatic browning in apple and apple products that is, phenolic compounds, polyphenoloxidases, and other factors (ascorbic acid and peroxidases), both qualitatively and quantitatively. Then the relationships between intensity of browning and the browning parameters are discussed, including a paragraph on the methods used for browning evaluation. Finally, the different methods for the control of browning are presented.

Sycamore suspension cells (Acer pseudoplatanusL.) were grown in the presence of sublethal concentrations of copper (50 μM). During the first 5–6 days of treatment, growth was not affected, but cell respiration (coupled and uncoupled) declined to ∼60% of its normal value. This decline of respiration was attributed to a progressive diminution of the number of mitochondria in copper‐treated cells, based on the demonstration of the concomitant decline of (1) cardiolipin (diphosphatidylglycerol) and cytochrome aa3(cytochrome oxidase), two specific markers of mitochondrial inner membrane, and (2) fumarase activity, a specific marker of mitochondrial matrix space. In addition, the mitochondria extracted from copper‐treated cells presented the same properties as those from control cells, concerning substrate oxidation, cardiolipin and cytochrome aa3contents, and fumarase activity. These results strongly suggest that copper triggered an arrest of mitochondrial biogenesis, which preceded cell division arrest.

Sycamore suspension cells ( Acer pseudoplatanus L.) were used to investigate the effect of copper on respiratory electron transport. Alternative oxidase (AOX) protein content and enzymatic capacity increased as a function of the concentration of copper added to the culture medium, from 0.2 to 50 μM. The latter sublethal concentration, which arrests mitochondrial biogenesis and thereby decreases cell respiration rates, stimulated cyanide-insensitive oxygen uptake in cells and mitochondria isolated therefrom. This was correlated with the accumulation of two proteins (30 and 36 kDa) which reacted with monoclonal antibodies against AOX. An accumulation of a 1.6-kb AOX mRNA was also observed. The possible mechanisms through which copper affects AOX are discussed.

Sycamore suspension cells (Acer pseudoplatanusL.) were incubated in the presence of sulfonylurea and imidazolinone herbicides. These inhibitors of acetolactate synthase (ALS), a key enzyme of branched‐chain amino acid synthesis, triggered a dramatic induction of the alternative oxidase (AOX). AOX activity increased in treated cells, eventually exceeding cytochrome (cyt) pathway activity. This induction of AOX activity was correlated with the accumulation of a 35 kDa AOX protein in isolated mitochondria, detected by Western blotting with a monoclonal antibody against Sauromatum guttatumAOX. It was preceded by the accumulation of putative 1.6 kb AOXmRNA, detected using an AoxcDNA probe from soybean. The metabolic perturbations induced by the herbicides rather than the herbicide molecules themselves were responsible for this induction of AOX. However, α‐oxobutyrate (one of the substrates of ALS) and its transamination product, α‐aminobutyrate, which accumulated after herbicide treatment, were not involved. The inhibition of branched‐chain amino acid synthesis was probably somehow responsible for the AOX induction since: (i) a mixture of those amino acids (leucine, isoleucine, valine) prevented AOX induction by ALS inhibitors; (ii) the herbicide Hoe 704, a potent inhibitor of acetolactate reducto‐isomerase (the enzyme following ALS in the branched‐chain amino acid pathway), also triggered AOX induction.