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 Na(2)MoO(4) 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 Na(2)MoO(4), 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 Na(2)MoO(4). Evidently, molybdenum toxicity in Chinese cabbage was not due to the direct interference of molybdate with the uptake and subsequent metabolism of sulphate.