Effects of nitric oxide-releasing nanoparticles on neotropical tree seedlings submitted to acclimation under full sun in the nursery.

Polymeric nanoparticles have emerged as carrier systems for molecules that release nitric oxide (NO), a free radical involved in plant stress responses. However, to date, nanoencapsulated NO donors have not been applied to plants under realistic field conditions. Here, we verified the effects of free and nanoencapsulated NO donor, S-nitroso-mercaptosuccinic acid (S-nitroso-MSA), on growth, physiological and biochemical parameters of neotropical tree seedlings kept under full sunlight in the nursery for acclimation. S-nitroso-MSA incorporation into chitosan nanoparticles partially protected the NO donor from thermal and photochemical degradation. The application of nanoencapsulated S-nitroso-MSA in the substrate favoured the growth of seedlings of Heliocarpus popayanensis, a shade-intolerant tree. In contrast, free S-nitroso-MSA or nanoparticles containing non-nitrosated mercaptosuccinic acid reduced photosynthesis and seedling growth. Seedlings of Cariniana estrellensis, a shade-tolerant tree, did not have their photosynthesis and growth affected by any formulations, despite the increase of foliar S-nitrosothiol levels mainly induced by S-nitroso-MSA-loaded nanoparticles. These results suggest that depending on the tree species, nanoencapsulated NO donors can be used to improve seedling acclimation in the nursery.

Studies of the inhibitory activities of tiopronin and mercaptosuccinic acid on glutathione peroxidase and their cytotoxic and antioxidant properties.

Glutathione peroxidase (GPx), an important antioxidative enzmye, can be inhibited by various thiols, including of tiopronin and mercaptosuccinic acid (MSA). Recently, there has been discussion regarding the combination of tiopronin in anticancer therapy to overcome acquired resistance to anticancer drugs. However, thiols are also known to act as antioxidants, which can be contraindicated in cancer chemotherapy. This article focuses on the inhibitory effects of tiopronin and MSA on bovine and human glutathione peroxidase activities, and their effects on the redox status of cancer cells. IC50 values for the inhibition for the bovine erythrocyte enzyme were 356 and 24.7 µM for tiopronin and MSA, respectively, with the corresponding Ki values of 343 µM and 14.6 µM, respectively at pH 7.4 and 25 °C. MSA inhibited human GPx activity in human cancer cell lysates at its IC50 while tiopronin did not. Both compounds were cytotoxic to human cancer cell lines GUMBUS and HL-60, with IC50 values between 42.7 and 149.4 µM. Neither had an effect on cell cycle. Only MSA induced apoptosis in HL-60 cells but not in GUMBUS cells, while tiopronin resulted in no apoptosis in either cell line. Combination studies of the MSA with hydrogen peroxide in living cells enhanced the production of reactive oxygen species in GUMBUS cells while tiopronin acted as antioxidant in HL-60 cells. MSA and tiopronin antagonized the cytotoxic effect of cisplatin, doxorubicin and methotrexate in combination studies. Our findings indicate that the antioxidant properties of both thiols prevail over their GPx inhibitory activity in human cancer cell lines.

Epithelial deposition of gold in the cornea in patients receiving systemic therapy.

Epithelial gold deposits were demonstrated biomicroscopically in 13 of 15 patients receiving gold therapy for rheumatoid arthritis. Only one of six further patients who had received gold therapy in the past showed such deposits. Deposits appeared with a cumulative dose of sodium thiomalate exceeding 100 mg. The earliest appearance was after seven months of therapy and deposits were visible in one subject as long as nine months after therapy had stopped. The density of deposit does not appear to increase over the whole of the dose range, possibly as a result of the effect of epithelial turnover. No symptoms attributable to the deposit were encountered in any patient.

Effect of gold on the immune response of mice.

Separate concurrent injection of organic gold compounds and antigen into mice resulted in immunoenhancement that could be measured by direct and indirect plaque-forming cells, rosette-forming cells, and serum antibody assays. Kinetics of the immune response showed variable effects through day 9 of the experiment. Studies with British anti-lewisite, a gold antagonist, showed that the gold must stay in the system 1 day to obtain immunoenhancement.