Molybdate toxicity in Chinese cabbage is not the direct consequence of changes in sulphur metabolism.

In polluted areas, plants may be exposed to supra-optimal levels of the micronutrient molybdenum. The physiological basis of molybdenum phytotoxicity is poorly understood. Plants take up molybdenum as molybdate, which is a structural analogue of sulphate. Therefore, it is presumed that elevated molybdate concentrations may hamper the uptake and subsequent metabolism of sulphate, which may induce sulphur deficiency. In the current research, Chinese cabbage (Brassica pekinensis) seedlings were exposed to 50, 100, 150 and 200 µm Na2 MoO4 for 9 days. Leaf chlorosis and a decreased plant growth occurred at concentrations ≥100 µm. Root growth was more affected than shoot growth. At ≥100 µm Na2 MoO4 , the sulphate uptake rate and capacity were increased, although only when expressed on a root fresh weight basis. When expressed on a whole plant fresh weight basis, which corrects for the impact of molybdate on the shoot-to-root ratio, the sulphate uptake rate and capacity remained unaffected. Molybdate concentrations ≥100 µm altered the mineral nutrient composition of plant tissues, although the levels of sulphur metabolites (sulphate, water-soluble non-protein thiols and total sulphur) were not altered. Moreover, the levels of nitrogen metabolites (nitrate, amino acids, proteins and total nitrogen), which are generally strongly affected by sulphate deprivation, were not affected. The root water-soluble non-protein thiol content was increased, and the tissue nitrate levels decreased, only at 200 µm Na2 MoO4 . Evidently, molybdenum toxicity in Chinese cabbage was not due to the direct interference of molybdate with the uptake and subsequent metabolism of sulphate.

Copper toxicity in Chinese cabbage is not influenced by plant sulphur status, but affects sulphur metabolism-related gene expression and the suggested regulatory metabolites.

The toxicity of high copper (Cu) concentrations in the root environment of Chinese cabbage (Brassica pekinensis) was little influenced by the sulphur nutritional status of the plant. However, Cu toxicity removed the correlation between sulphur metabolism-related gene expression and the suggested regulatory metabolites. At high tissue Cu levels, there was no relation between sulphur metabolite levels viz. total sulphur, sulphate and water-soluble non-protein thiols, and the expression and activity of sulphate transporters and expression of APS reductase under sulphate-sufficient or-deprived conditions, in the presence or absence of H2 S. This indicated that the regulatory signal transduction pathway of sulphate transporters was overruled or by-passed upon exposure to elevated Cu concentrations.

The characteristic high sulfate content in Brassica oleracea is controlled by the expression and activity of sulfate transporters.

The uptake and distribution of sulfate in BRASSICA OLERACEA, a species characterised by its high sulfate content in root and shoot, are coordinated and adjusted to the sulfur requirement for growth, even at external sulfate concentrations close to the K (m) value of the high-affinity sulfate transporters. Plants were able to grow normally and maintain a high sulfur content when grown at 5 or 10 microM sulfate in the root environment. Abundance of mRNAs for the high affinity sulfate transporters, BolSultr1;1 and BolSultr1;2, were enhanced at

Atmospheric H(2)S as sulfur source for Brassica oleracea: kinetics of H(2)S uptake and activity of O-acetylserine (thiol)lyase as affected by sulfur nutrition.

The uptake of hydrogen sulfide (H(2)S) by shoots of curly kale (Brassica oleracea) showed saturation kinetics with respect to the atmospheric concentration. The kinetics are largely determined by the rate of metabolism of the absorbed H(2)S into cysteine, catalyzed by O-acetylserine (thiol)lyase, and can be described by the Michaelis-Menten equation. When B. oleracea was grown under sulfate (SO(4)(2-))-deprived conditions, plants developed sulfur (S) deficiency symptoms and H(2)S uptake kinetics were substantially altered. Shoots of SO(4)(2-)-deprived plants had a lower affinity to H(2)S uptake, whereas the maximal H(2)S uptake rate was higher. When SO(4)(2-)-deprived plants were simultaneously exposed to 0.2 &mgr;l l(-1) H(2)S all S deficiency symptoms disappeared and H(2)S uptake kinetics returned rapidly to values observed for S-sufficient shoots. The activity of the H(2)S-fixating enzyme O-acetylserine (thiol)lyase was hardly affected upon either prolonged H(2)S exposure or SO(4)(2-) deprivation. Evidently, the activity of O-acetylserine (thiol)lyase was not the rate-limiting step in the H(2)S uptake by shoots. The significance of the in situ availability and rate of synthesis of the substrate O-acetylserine for O-acetylserine (thiol)lyase as determining factor in the uptake kinetics of H(2)S needs further evaluation.