Search

Methylmercury (MeHg) is an organic form of mercury with toxic effects in multiple organs. The aim of the present investigation was to evaluate the in vivo effects of MeHg (1 and 4 mg/kg) given orally for seven consecutive days on adenosine deaminase (ADA), n-acetyl-β-D-glucosaminidase (NAG) and ecto-nucleoside triphosphate phosphohydrolase (NTPDase) activities, and on lipid peroxidation in hippocampus, cerebral cortex, kidney and liver of suckling rat pups. The results showed that NAG activity and lipid peroxidation levels increased in the kidney in both treatments, whereas urinary NAG activity increased only in the 1 mg/kg treatment. Despite the fact that the lipid peroxidation increased in both cerebral cortex and hippocampus, the latter appeared to be more vulnerable to MeHg exposure as it also had an increase in ADA activity. Thus, although dietary MeHg modified renal cell function, it did not alter histological features in suckling rat pups. The results of our investigation are of significant importance because they demonstrated responses to exposition to low doses of MeHg in target organs during the development of the rat. Especially the kidney was affected by the oral exposure to MeHg, suggesting the vulnerability of this organ at this stage of development. Moreover, the urinary NAG may provide important data that could serve as basis for risk assessment purposes following MeHg exposure.

Selenium (Se) is a dietary essential trace element with important biological roles. Sodium selenate (Na(2)SeO(4)) is an inorganic Se compound used in human and animal nutrition that acts as precursor for selenoprotein synthesis. The organoselenium 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one (C(21)H(2)HOSe) is an α,β-unsaturated ketone functionalized vinyl chalcogenide that has been found as a potential tool in organic synthesis. Adenosine deaminase (ADA) is an important enzyme in the degradation of adenine nucleotides. In this study, we investigated the in vitro effects of both Se compounds on ADA activity and cell viability in leukocyte suspension (LS) of healthy donors (n=12). We first observed an inhibition of ADA activity using 0.1 μM of 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one, and an increase in cellular viability when 30 μM were used. However, we did not observe alterations in the presence of sodium selenate. Moreover, both Se compounds did not alter lactate dehydrogenase activity and thiobarbituric acid reactive substance levels. These results suggest that the inhibition of ADA activity caused by α,β-unsaturated ketone may affect the adenosine levels in LS and modulate cell viability, attenuating conditions that involve the activation of the immune system.

The study was undertaken to evaluate changes in the activity of adenosine deaminase (ADA) in brains of rats infected by Trypanosoma evansi. Each rat was intraperitoneally infected with 10(6) trypomastigotes either suspended in fresh (group A; n = 13) and cryopreserved blood (group B; n = 13). Thirteen animals were used as control (group C). ADA activity was estimated in the cerebellum, cerebral cortex, striatum and hippocampus. No differences (P0.05) in ADA activity were observed in the cerebellum between infected and non-infected animals. Significant (P0.05) reductions in ADA activity occurred in cerebral cortex in acutely (day 4 post-infection; PI) and chronically (day 20 PI) infected rats. ADA activity was significantly (P0.05) decreased in the hippocampus in acutely infected rats, but significantly (P0.05) increased in the chronically infected rats. Significant (P0.05) reductions in ADA activity occurred in the striatum of chronically infected rats. Parasites could be found in peripheral blood and brain tissue through microscopic examination and PCR assay, respectively, in acutely and chronically infected rats. The reduction of ADA activity in the brain was associated with high levels of parasitemia and anemia in acute infections. Alterations in ADA activity of the brain in T. evansi-infected rats may have implications for pathogenesis of the disease.

Adenosine deaminase (ADA) is involved in purine metabolism and plays a significant role in the immune system. The focus of this investigation was to examine the effects of low concentrations of organic mercury on ADA activity in human leukocytes and to investigate the relationship between these effects and cell death. We have examined the protective potential effects of Allium sativum extract (GaE) against Methylmercury (MeHg)-induced cytotoxic effects on human leucocytes under in vitro conditions. MeHg (0.05-10 microM) significantly decreased leukocyte viability (58.97% for MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) and 51.67% for Alamar Blue (AB) and this decrease was positively correlated to the MeHg-induced inhibition of ADA activity. N-acetylcysteine (NAC) and GaE prevented both the MeHg-induced cytotoxic effects on leukocytes according to MTT and AB assays and the effects on the ADA activity. The present results suggest that the protective effects of GaE against MeHg-induced leukocyte damage is related to the removal of oxidant species generated in the presence of MeHg due to the antioxidant efficacy of garlic constituents. It is important to point out that the intense presence of ADA in Leukocyte suspension (LS) highlights the relevant effects in the immune system and in vitro cytotoxicity of MeHg exposure.

A reversed-phase high-performance liquid chromatographic method has been developed and validated for quantitative determination of deflazacort in tablets and in compounded capsules. Isocratic chromatography was performed on a C18 column with acetonitrile–water 80:20 (v/v) as mobile phase at a flow rate of 1.0 mL min−1. UV detection was at 240 nm. The linearity of the method was good (r > 0.999), as also were intra-day and inter-day precision (RSD 98%). The method was also validated for specificity and robustness. The results showed the proposed method is suitable for its intended use.