Dengue virus-induced cytotoxin releases nitrite by spleen cells

Dengue type-2 virus (DV) infection in mice induces T cells to produce a cytokine, the cytotoxic factor (CF), which induces H2-A positive macrophages to produce another cytokine, cyotoxin (CF2), which amplifies its cytotoxic effects on target cells. The present study was undertaken to investigate the production of nitrite (NO−2) by the spleen cells of mice in vitro and in vivo following inoculation of CF2. Maximum NO−2 production occurred at 1 hour after inoculation of 100 μg CF2. Pretreatment of CF2 with anti-CF2-antisera (CF2-As) inhibited the production of NO−2. Pretreatment of the spleen cells with NG-monomethyl- l-arginine (NMA) or with arginase inhibited NO−2 production. The NO−2 production was diminished in a dose dependent manner by treatment of spleen cells with the Ca2+ channel blocking drug, nifedipine and Zn2+ as ZnSO4. The findings of the present study thus demonstrate that CF2 induces production of NO−2 in the spleen cells in a CA2+-dependent manner which may be a mechanism of target cell killing

Release of reactive oxygen intermediates by dengue virus-induced macrophage cytotoxin

Dengue type 2 virus (DV) induces a subpopulation of T lymphocytes of mice to produce a cytokine, cytotoxic factor (mCF), which induces H-2A positive macrophages to produce macrophage cytotoxin (CF2). The present study was undertaken to investigate the mechanism of cytotoxicity of CF2. It was observed that CF2 induced production of superoxide anion (O−2) and hydrogen peroxide (H2O2) by the spleen cells of mice in vitro and in vivo. The maximum production of O−2 (260 ±10 n M/4 × 106 cells) was at 45 minutes while that of H2O2 was at 90 minutes after inoculation of CF2. Pretreatment of mice or spleen cells with anti-CF2-antisera inhibited O−2 and H2O2 production in a dose-dependent manner. Superoxide dismutase (SOD) inhibited O−2 production and cytotoxicity while H2O2 production was increased by increasing SOD concentration in the culture. This indicated that O−2 production is necessary for the cytotoxic activity of CF2. Pretreatment of the cells with Ca2+ channel blocking drugs, nifedipine or verapamil, inhibited CF2-induced O−2 and H2O2 production in a dose-dependent manner. We have shown earlier that the cytotoxic activity of CF2 is known to be Ca2+ dependent and CF2-induced production of nitrite and the cytotoxicity is inhibited by NG-monomethyl- L-arginine. Thus, it is suggested that O−2 and nitrite are necessary for cell killing by CF2 in a Ca2+ manner and the killing may possibly be by generation of peroxynitrite

Abiotic stresses, constraints and improvement strategies in chickpea

Chickpea (Cicer arietinum L.) is cultivated mostly in the arid and semi-arid regions of the world. Climate change will bring new production scenarios as the entire growing area in Indo–Pak subcontinent, major producing area of chickpea, is expected to undergo ecological change, warranting strategic planning for crop breeding and husbandry. Conventional breeding has produced several high-yielding chickpea genotypes without exploiting its potential yield owing to a number of constraints. Among these, abiotic stresses include drought, salinity, water logging, high temperature and chilling frequently limit growth and productivity of chickpea. The genetic complexity of these abiotic stresses and lack of proper screening techniques and phenotyping techniques and genotype-by-environment interaction have further jeopardized the breeding programme of chickpea. Therefore, considering all dispiriting aspects of abiotic stresses, the scientists have to understand the knowledge gap involving the physiological, biochemical and molecular complex network of abiotic stresses mechanism. Above all emerging ‘omics’ approaches will lead the breeders to mine the ‘treasuring genes’ from wild donors and tailor a genotype harbouring ‘climate resilient’ genes to mitigate the challenges in chickpea production