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.

High mobility group box1 (HMGB1) in relation to cutaneous inflammation in systemic lupus erythematosus (SLE).

SUMMARY: Photosensitivity is characteristic of systemic lupus erythematosus (SLE). Upon ultraviolet B (UVB) exposure, patients develop inflammatory skin lesions in the vicinity of sunburn cells (SBCs). High mobility group box 1 (HMGB1) is released from apoptotic and activated cells and exerts inflammatory actions through ligation to its receptors. METHODS: Eleven SLE patients and 10 healthy controls (HCs) were exposed to UVB. Skin biopsies were taken before and at one, three and 10 days after irradiation. Sections were stained for SBC, HMGB1, CD3, CD68, interferon-induced protein MxA and cleaved caspase 3. In vitro experiments with UVB-irradiated keratinocytes were also performed. Higher numbers of cells that had released HMGB1 were seen in the skin of SLE patients compared to HCs before and after irradiation. HMGB1-negative nuclei correlated with the presence of SBCs, and with the number of cleaved caspase 3 positive cells in lupus skin. RESULTS: HMGB1 release is increased in the skin of SLE patients compared to HCs. Upon UVB exposure, HMGB1 release further increases in SLE patients and is related to the number of apoptotic cells. Our data suggest that HMGB1, probably released from apoptotic keratinocytes, contributes to the development of inflammatory lesions in the skin of SLE patients upon UVB exposure.