ABSTRACT
Objective To evaluate whether hypoxia inducible factor (HIF-1α) targeting pharmacological drugs, echinomycin, resveratrol and CdCl
ABSTRACT
OBJECTIVE@#To evaluate whether hypoxia inducible factor (HIF-1α) targeting pharmacological drugs, echinomycin, resveratrol and CdCl2 which inhibit HIF-1α stimulation, and mimosine, which enhances the stability of HIF-1α present antileishmanial properties.@*METHODS@#The leishmanicidal effect of drugs was evaluated in mouse macrophages and Balb/c mouse model for cutaneous leishmaniosis.@*RESULTS@#Resveratrol and CdCl2 reduced the parasite load [IC50, (27.3 ± 2.25) μM and (24.8 ± 0.95) μM, respectively]. The IC50 value of echinomycin was (22.7 ± 7.36) nM and mimosine did not alter the parasite load in primary macrophages. The macrophage viability IC50 values for resveratrol, echinomycin and CdCl2 and mimosine were >40 μM, >100 nM, >200 μM and>2000 μM, respectively. In vivo no differences between cutaneous lesions from control, resveratrol- and echinomycin-treated Balb/c mice were detected.@*CONCLUSIONS@#Resveratrol, echinomycin and CdCl2 reduce parasite survival in vitro. The HIF-1α targeting pharmacological drugs require further study to more fully determine their anti-Leishmania potential and their role in therapeutic strategies.
ABSTRACT
Salt stress as a major adverse factor can lower leaf water potential, leading to reduced torgor and some other responses, and ultimately lower crop productivity in arid and semi arid zone. Plant responses to salt stress have much in common. Salt stress reduces the ability of plants to take up water and this quickly causes reductions in growth rate. The initial reduction in shoot growth is probably due to salt effects. If excessive amounts of salt enter into the plant, salt will eventually rise to toxic levels and reduce the photosynthetic leaf area of the plant that cannot sustain growth. In order to understand the processes that give rise to tolerance of salt and to identify the salt stress proteins in the salt stress effect of on plant growth was studied using different salt solutions like Copper sulphate, Cadmium chloride and zinc sulphate with different concentrations like 200μM, 150μM, 100μM.
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Objective To investigate cadmium induced adaptive responses (AR) to either toxicant challenge or irradiation and also the role of PI3K family in the AR. Methods Cells were pre-treated with 0.1 or 1 μmol/L cadmium and then challenged by 50, 100 μmol/L cadmium or 1, 2 Gy γ-rays irradiation. Micronucleus induction was measured to evaluate the magnitude of AR. In some experiments, cells were treated with wortmannin during and after pretreatment. Results Cadmium of sub-lethal concentration could induce AR in all the cells toward 50 μmol/L cadmium or 1 Gy irradiation. When challenged by 50 μmol/L CdCl1, EM-C11 cells had an AR less apparent than the other two cell lines. Moreover, treatment of cells with wortmannin eliminated the AR in all three cell lines. Conclusions The magnitudes of AR in adapted cells may be related to multiple factors, such as DNA repair capacity, the priming and challenging dose of cadmium or irradiation. SSB rather than DSB repair is mainly involved in the cadmium induced AR and this cellular response may be mediated through ATM pathway.
ABSTRACT
Cadmium (Cd) affects cell proliferation, differentiation, apoptosis and other cellular activities and can cause numerous molecular lesions that would be relevant to carcinogenesis. The mechanism of adverse effects of Cd has been poorly understood and, especially on the tight junction. Since there is rare information about the effect of Cd on tight junction protein, we here investigated whether Cd can alter the localization of the proteins. This study examined Cd effects on of tight junction (occludin, ZO-1, and ZO-2) using MDCK cell culture. The change of MDCK cell and tight junction was investigated after treatment of cadmium with phase contrast microscopy, TEER, cell viability, Transmission electron microscopy and confocal laser microscopy. After treatment of cadmium, transendothelial electrical resistance decreased with time and concentration dependent manner. AlamarBlue assay revealed that decreased cell viability also decreased with time and concentration dependent manner. The tight junction moved down between intercellular spaces with decreased density and the cellular thickness around cell junctions decreased with increasing concentration and exposure time of CdCl2. The MDCK cells eventually showed cell death with. Confocal laser microscopy revealed that immunofluorescent reaction of occludin, ZO-1 and ZO-2 decreased. Occludin, ZO-1 and ZO-2 were disrupted at tight junction. These data suggest that after treatment of Cd, increased permeability of MDCK cell monolayer increased. This might be accompanied with disruption of occludin, ZO-1 and ZO-2.