Inhibition of selenium dependent glutathione peroxidase and superoxide dismutase in rats by diethyldithiocarbamate: Effect of pre-administration of <img src='/image/spc_char/alpha.gif'> -tocopherol

465-468Rats pre-administered with -tocopherol (10 mgs/day) for 7 days afforded a significant protection at the tissue level against the lowering of superoxide dismutase and glutathione peroxidase, especially the selenium-dependent glutathione peroxidase. The protective action of -tocopherol in the diethyldithiocarbamate treated rats may be attributed to its antioxidant/free radical scavenging action. It is concluded that selenium-dependent glutathione peroxidase and -tocopherol act in a complementary fashion to block free radical formation

Infection induced oxidative cross-linking of hydroxyproline-rich glycoproteins (HRGPs) is associated with restriction of <i>Colletotrichum sublineolum</i> in sorghum

Hydroxyproline-rich glycoproteins (HRGPs) accumulation and oxidative cross-linking is one of the earliest defense responses in plants against pathogen infection. In the present study HRGP accumulation in three sorghum genotypes i.e. SC146 (resistant), cv. SC326 (intermediately resistant) and BTx623 (susceptible) as a response to Colletotrichum sublineolum isolate CP2126 infection is elucidated. HRGPs were monitored by hydroxyproline (Hyp) estimation. In genotypes SC146 and genotypes SC326 there was a significantly higher amounts of Hyp at 2 days after inoculation (dai) compared to genotype BTx623, indicating an infection induced accumulation of HRGPs. Western blot analysis of acid-ethanol extracted proteins with polyclonal antibody raised against pearl millet purified HRGPs identified four bands with molecular masses of ~65, 45, 17 and 14 kDa as HRGPs. Insolubilization of the 45 kDa protein in genotypes SC146 and SC326 upon infection with C. sublineolum indicates a role of this protein in cell wall cross-linking, coinciding with heavier accumulation of hydrogen peroxide. In addition, tissue print analysis using polyclonal antibody of pearl millet HRGPs recognized these cross-linked proteins to be HRGPs. These findings indicated that HRGPs in sorghum is a component of defense reaction against C. sublineolum infection

Infection induced oxidative cross-linking of hydroxyproline-rich glycoproteins (HRGPs) is associated with restriction of colletotrichum sublineolum in sorghum

Hydroxyproline-rich glycoproteins (HRGPs) accumulation and oxidative cross-linking is one of the earliest defense responses in plants against pathogen infection. In the present study HRGP accumulation in three sorghum genotypes i.e. SC146 (resistant), SC326 (intermediately resistant) and BTx623 (susceptible) as a response to Colletotrichum sublineolum isolate CP2126 infection is elucidated. HRGPs were monitored by hydroxyproline (Hyp) estimation. In genotypes SC146 and SC326 there was a significantly higher amounts of Hyp at 2 days after inoculation (dai) compared to genotype BTx623, indicating an infection induced accumulation of HRGPs. Western blot analysis of acid-ethanol extracted proteins with polyclonal antibody raised against pearl millet purified HRGPs identified four bands with molecular masses of similar to 65, 45, 17 and 14 kDa as HRGPs. Insolubilization of the 45 kDa protein in genotypes SC146 and SC326 upon infection with C. sublineolum indicates a role of this protein in cell wall cross-linking, coinciding with heavier accumulation of hydrogen peroxide. In addition, tissue print analysis using polyclonal antibody of pearl millet HRGPs recognized these cross-linked proteins to be HRGPs. These findings indicated that HRGPs in sorghum is a component of defense reaction against C. sublineolum infection

Role of innate immunological/inflammatory pathways in myelodysplastic syndromes and AML: a narrative review

Abstract Dysregulation of the innate immune system and inflammatory-related pathways has been implicated in hematopoietic defects in the bone marrow microenvironment and associated with aging, clonal hematopoiesis, myelodysplastic syndromes (MDS), and acute myeloid leukemia (AML). As the innate immune system and its pathway regulators have been implicated in the pathogenesis of MDS/AML, novel approaches targeting these pathways have shown promising results. Variability in expression of Toll like receptors (TLRs), abnormal levels of MyD88 and subsequent activation of NF-κβ, dysregulated IL1-receptor associated kinases (IRAK), alterations in TGF-β and SMAD signaling, high levels of S100A8/A9 have all been implicated in pathogenesis of MDS/AML. In this review we not only discuss the interplay of various innate immune pathways in MDS pathogenesis but also focus on potential therapeutic targets from recent clinical trials including the use of monoclonal antibodies and small molecule inhibitors against these pathways