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Three novel organotellurium (IV) derivatives of diphenyldithiocarbamate, C4H8Te[(CS2) N(C6H5)2]2(1), (C2H5)2Te[(CS2) N(C6H5)2]2(2), and C4H7(CH3)Te[(CS2) N(C6H5)2]2(3) have been synthesized by the reaction of sodium salt of diphenyl dithiocarbamate with C4H8TeI2, (C2H5)2TeI2, and C4H7(CH3)TeI2 respectively. The synthesized compounds 1–3 were characterized by elemental analysis, IR, 1H NMR, and 13C{1H} NMR spectroscopic studies. The antimicrobial efficacy of compounds 1–3 was examined against selected bacterial and fungal strains using broth microdilution and disc diffusion methods. Penicillin and amphotericin B were used as a positive control for bacterial and fungal strains respectively. The highest activity against bacterial strains was shown by compound 3 while against the fungal strain compound 1 showed the highest activity with a MIC value of 6.25 µg/ml. However, all compounds showed high to moderate antimicrobial activity. [ABSTRACT FROM AUTHOR]

Silver (Ag) and gold nanoparticles (Au NPs) have wide applications. They are increasingly being used in the medical devices, biosensors, cancer cell imaging, and cosmetics. Increased applications of these NPs in the technological advances have also led to the risk of exposure to these particles. This study investigated the toxic effects of Ag and Au NPs (1 μM and 2 μM, oral) on mouse erythrocytes and tissues after 14 consecutive days’ exposure. Our results demonstrate significant increase in reactive oxygen species (ROS) and depletion of antioxidant enzyme status in erythrocytes and tissues. Hepatic and renal toxicity was evident from liver and kidney function tests. Inflammatory markers, interleukin-6 and nitric oxide synthase increased in plasma on administration following exposure to these NPs at both the doses. A more pronounced increase was noted in kidney metallothionein (MT) compared to liver MT on exposure to these NPs. Toxic potential of these NPs was further confirmed by increased 8-hydroxy-2′-deoxyguanosine levels in urine, a biomarker of DNA damage. Among the two NPs, Ag NP was more toxic at 2 μM dose compared to lower dose of 1 μM. The study suggests oxidative stress as the major mechanism responsible for the toxic manifestations induced by Ag and Au NPs. [ABSTRACT FROM AUTHOR]

Nanomaterials are at the leading edge of the rapidly developing field of nanotechnology. However the information regarding toxicity of these nanoparticles on humans and environment is still deficient. The present study investigated the toxic effects of three metal oxide nanoparticles, TiO2, ZnO and Al2O3 on mouse erythrocytes, brain and liver. Male mice were administered a single oral dose of 500 mg/kg of each nanoparticles for 21 consecutive days. The results suggest that exposure to these nano metallic particles produced a significant oxidative stress in erythrocyte, liver and brain as evident from enhanced levels of Reactive Oxygen Species (ROS) and altered antioxidant enzymes activities. A significant increase in dopamine and norepinephrine levels in brain cerebral cortex and increased brain oxidative stress suggest neurotoxic potential of these nanoparticles. Transmission electron microscopic (TEM) analysis indicated the presence of these nanoparticles inside the cytoplasm and nucleus. These changes were also supported by the inhibition of CuZnSOD and MnSOD, considered as important biomarkers of oxidative stress. The toxic effects produced by these nanoparticles were more pronounced in the case of zinc oxide, followed by aluminum oxide and titanium dioxide, respectively. The present results further suggest the involvement of oxidative stress as one of the main mechanisms involved in nanoparticles induced toxic manifestations. [ABSTRACT FROM AUTHOR]

The individual toxic effects of arsenic and organophosphate pesticides are known but there is a lack of data on their combined effects. The present study investigates the toxic effects following combined exposure to organophosphate and arsenic on: (i) alterations in brain biogenic amines, (ii) oxidative stress and its correlation with glutathione linked enzymes, cell death and histopathological observations, and (iii) arsenic concentration in soft tissues. Rats were exposed to arsenic (1 mg kg−1 body weight, orally) and dichlorvos (4 mg kg−1 body weight, subcutaneously) either individually or in combination for 16 weeks. Arsenic alone and in combination with DDVP led to a significant increase in reactive oxygen species (ROS), thiobarbituric acid reactive substance (TBARS), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities accompanied by a decreased glutathione reductase, reduced and oxidized glutathione (GSH and GSSG) levels in tissues. Arsenic and DDVP also produced a significant depletion in brain biogenic amines; however, acetylcholinesterase (AChE) activity increased moderately on arsenic exposure. Arsenic and DDVP co-exposure exhibited synergism in the case of ROS while no such effect was noted in the case of TBARS. Interestingly, combined exposure to arsenic and DDVP resulted in more pronounced toxic effects compared to their individual effects based on various biochemical variables, cell death (TUNEL assay) and histopathological observations. Interestingly, brain arsenic levels decreased on co-exposure to arsenic and DDVP accompanied with prominent elevation of liver arsenic content in co-exposed groups. The present study thus provides some interesting observations on the interaction between arsenic and DDVP including (i) co-exposure to arsenic and DDVP might lead to significant oxidative stress and (ii) their co-exposure produced synergistic effects on some liver variables but some antagonistic effects on the brain. [ABSTRACT FROM AUTHOR]

Dichlorvos (DDVP) and monocrotophos (MC) are systemic insecticides and known to produce cholinergic and non-cholinergic effects. Individual toxic effects of these chemicals are known but their combined effects have not been studied. We studied the effect of concomitant exposure to DDVP and MC on selected biochemical variables suggestive of liver damage, changes in whole brain biogenic amines levels, acetylcholinesterase (AchE) and monoamine oxidase (MAO) activities in rats. Female rats were exposed to DDVP (2.5 mg/kg subcutaneously) and MC (1.8 mg/kg oral) either individually or in combination for 4 weeks. We observed significant decrease in more pronounced depletion in norepinephrine (NE) and dopamine (DA) levels during co-exposure to DDVP and MC. Brain AChE activity increased and activity of MAO showed significant depletion on co-exposure to DDVP and MC. Brain glutathione (GSH) and oxidized glutathione (GSSG) ratio decreased significantly during exposure to DDVP or MC while co-exposure to these toxicants led to a more pronounced depletion of GSH: GSSG ratio. Serum aspartate amino transferase (AST) and alkaline phosphatase (ALP) activities increased significantly on exposure to MC suggesting liver injury, while DDVP alone had no effect on these variables. There were no effects of DDVP and MC exposure on haematological biochemical variables except for depletion in serum glucose level after MC exposure which was more pronounced DDVP + MC during co-exposure. It can be concluded that only moderate synergistic effects occur between MC and DDVP during co-exposure. A more detailed study with variable doses, prolonged exposure and alterations in different brain regions is recommended. [ABSTRACT FROM AUTHOR]

Nanomaterials are at the leading edge of the rapidly developing field of nanotechnology. However the information regarding toxicity of these nanoparticles on humans and environment is still deficient. The present study investigated the toxic effects of three metal oxide nanoparticles, TiO2, ZnO and Al2O3 on mouse erythrocytes, brain and liver. Male mice were administered a single oral dose of 500 mg/kg of each nanoparticles for 21 consecutive days. The results suggest that exposure to these nano metallic particles produced a significant oxidative stress in erythrocyte, liver and brain as evident from enhanced levels of Reactive Oxygen Species (ROS) and altered antioxidant enzymes activities. A significant increase in dopamine and norepinephrine levels in brain cerebral cortex and increased brain oxidative stress suggest neurotoxic potential of these nanoparticles. Transmission electron microscopic (TEM) analysis indicated the presence of these nanoparticles inside the cytoplasm and nucleus. These changes were also supported by the inhibition of CuZnSOD and MnSOD, considered as important biomarkers of oxidative stress. The toxic effects produced by these nanoparticles were more pronounced in the case of zinc oxide, followed by aluminum oxide and titanium dioxide, respectively. The present results further suggest the involvement of oxidative stress as one of the main mechanisms involved in nanoparticles induced toxic manifestations.