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The objective of this study was to evaluate Cr toxicity in young plants of the CCN 51 Theobroma cacao genotype at different concentrations of Cr 3+ in the soil (0, 100, 200, 400 and 600 mg kg -1 ) through physiological, ultrastructural, antioxidant and molecular changes. Doses of 400 and 600 mg Cr 3+ kg -1 soil severely affected foliar gas exchange, promoted by damages in photosynthetic machinery evidenced by the decrease in CO 2 fixation. Decreased expression of psbA and psbO genes, changes in enzymatic activity and lipid peroxidation also affected leaf gas exchange. A hormesis effect was observed at 100 mg Cr 3+ kg -1 soil for the photosynthetic activity. As a metal exclusion response, the roots of the cocoa plants immobilized, on average, 75% of the total Cr absorbed. Ultrastructural changes in leaf mesophyll and roots, with destruction of mitochondria, plasmolysis and formation of vesicles, were related to the oxidative stress promoted by excess ROS. The activity of the antioxidant enzymes SOD, APX, GPX and CAT and the amino acid proline coincided with the greater expression of the sod cyt gene demonstrating synchronicity in the elimination of ROS. It was concluded, therefore, that the tolerance of the cocoa plants to the toxicity of Cr 3+ depends on the concentration and time of exposure to the metal. Higher doses of Cr 3+ in the soil promoted irreversible damage to the photosynthetic machinery and the cellular ultrastructure, interfering in the enzymatic and non-enzymatic systems related to oxidative stress and gene expression. However, the low mobility of the metal to the leaf is presented as a strategy of tolerance to Cr 3+ ., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Plasmodium infection causes major losses to animal and human populations. The characterization of experimental malaria models is needed for a better understanding of disease mechanisms and the development of new treatment protocols. Chickens infected with Plasmodium gallinaceum constitute an adequate malaria model due to the phylogenetic proximity of this parasite to human Plasmodium as well as similarities in disease manifestation, such as cerebral malaria. The aim of the present study was to further characterize the experimental chicken model with an emphasis on clinical manifestations, cerebral histology and nitric oxide (NO) produced by macrophages. The results revealed that mortality was correlated to higher parasitemia. Parasitemia was positively correlated to temperature and negatively correlated to haematocrit value. Brain histology of infected birds revealed inflammatory infiltrates and blocked microvasculature. Macrophages derived from blood monocytes produced NO after activation, with a higher production positively correlated to parasitemia. These results characterize histological aspects of chicken brain malaria and demonstrate the activation of the innate immune system caused by the infection in chickens., ((c) 2010 Elsevier B.V. All rights reserved.)

Thiamethoxam is a neonicotinoid insecticide, a group of pesticides that acts selectively on insect nicotinic acetylcholine receptors (nAChRs), with only a little action on mammalian nAChRs. Nevertheless, the selectivity of neonicotinoids for the insect nAChRs may change when these substances are metabolized. Therefore, we aimed to determine the potential effects of thiamethoxam on mammalian brain, testing the performance in the open field and elevated plus-maze of rats exposed to this insecticide and, in order to establish the neurochemical endpoints, we measured the acetylcholinesterase activity in different brain regions (hippocampus, striatum and cortex) and the high-affinity choline uptake (HACU) in synaptosomes from rat hippocampus. Treated animals received thiamethoxam (25, 50 or 100mg/kg) for 7 consecutive days. The results showed that treatment with thiamethoxam induced an increase in the anxiety behavior at two doses (50 or 100mg/kg). Moreover, there was a significant decrease in both HACU and acetylcholinesterase activity. Our hypothesis is that thiamethoxam (or its metabolites) could be acting on the central rats nAChRs. This would produce an alteration on the cholinergic transmission, modulating the anxiety behavior, acetylcholinesterase levels and HACU.

Mercury compounds versatility explains their numerous applications in diverse areas of industry. The growing use of this metal has resulted in a significant increase of environment contamination and episodes of human intoxication, arousing the concern of international organisms. Meanwhile, consequences of these intoxication outbreaks are still not fully understood, especially if we consider long-term effects of chronic exposure to relatively low levels of mercury compounds. In the present manuscript, studies about the genotoxicity of mercury compounds, performed in vitro, in vivo, and/or including epidemiologic studies of human populations were reviewed. Some mercury compounds are known as teratogenic agents, especially affecting the normal development of the central nervous system; however, the connection between mercury exposure and carcinogenesis remains controversial. Since 1990s, epidemiological studies have begun to include an increasing number of human subjects, making the results more reliable: thus, increased genotoxicity was demonstrated in human populations exposed to mercury through diet, occupation or by carrying dental fillings. In fact, concentrations of methylmercury causing significant genotoxic alterations in vitro below both safety limit and concentration were associated with delayed psychomotor development with minimal signs of methylmercury poisoning. Based on mercury's known ability to bind sulfhydryl groups, several hypotheses were raised about potential molecular mechanisms for the metal genotoxicity. Mercury may be involved in four main processes that lead to genotoxicity: generation of free radicals and oxidative stress, action on microtubules, influence on DNA repair mechanisms and direct interaction with DNA molecules. All data reviewed here contributed to a better knowledge of the widespread concern about the safety limits of mercury exposure.

Mercury is a hazardous metal that has become an important issue of environmental contamination in Amazon areas. Human intoxication by mercury causes sensory deficits, motor dysfunction, delayed psychomotor development, genotoxicity, and several other health problems. One of the major cellular mechanisms of mercury toxicity is the oxidative stress which may lead to membrane peroxidation and generation of reactive oxygen species. The antioxidant defense, which includes scavenger compounds such as glutathione and antioxidant enzymes such as catalase, might prevent these injuries to occur. Thus, the objective of this work was to evaluate hair mercury levels and the strength of antioxidant defenses, evaluated by glutathione levels and catalase activity in the blood of exposed and non-exposed women living in Amazon populations. For each location, no statistically significant difference (P<0.05) was detected for age versus mercury content. However, women from populations under the influence of gold mining activity exhibit high mercury levels in hair samples, above the tolerance limit accepted by the World Health Organization. In addition, a significant correlation was found between high mercury content, high glutathione level, and lower catalase activity. These data suggest that chronic mercury intoxication may deplete antioxidant enzymatic activity, which can be used as an important peripheral marker. Knowledge originated by this monitoring will better assist the development of preventive strategies and governmental actions against the problem of mercury contamination.

Methylmercury (MeHg) is related to several deleterious effects on the vertebrate nervous system and part of these effects are through interaction with sulfhydryl (-SH) group found in cellular proteins. We decided to characterize the dose-dependent effect of MeHg on the neurotoxicity and the neurite outgrowth induced effects on chick sympathetic neurons dissociated and purified in culture. In this model, MeHg inhibited neurite outgrowth (1-10 microM) and induced cell death (1-10 microM) after 48 h in culture. Since metal toxicity often generates reactive oxygen species, we tested if antioxidant compounds such as glutathione (GSH) or L-cysteine (L-cys) could block the deleterious effects promoted by MeHg. L-methionine, another sulfur-containing amino acid, but without a SH group, was also used in this work. We show that GSH (10-100 microM) and L-cys (100 microM), but not L-methionine (100 microM), fully blocked neurite degeneration and sympathetic neuron cell death in culture.

The aim of this research was to verify the incidence of endocrine dysfunction associated with mercury intoxication in the hypothalamus-pituitary reproductive system of normally cycling or castrated female rats and the possible protective action of estrogen replacement therapy. We found no differences in the frequency of estrus cycle stages (diestrus I, diestrus II, proestrus, and estrus) in normally cycling female rats during 54 days of daily oral administration of 0.004, 0.02, and 1 mg/kg MeHgCl. Conversely, the higher dose (1 mg/kg) induced a significant decrease in content of luteinizing hormone releasing hormone (LHRH) into the medial hypothalamus when administered daily during 3 days in ovariectomized rats. This effect was associated with increased levels of mercury found in the anterior pituitary gland and medial hypothalamus, rather than the anterior and posterior hypothalamus, striatum or cerebellum. A decrease in plasma levels of luteinizing hormone (LH) was also detected after administration of 7.5 mg/kg MeHgCl. These disturbances in LHRH and LH secretion induced by mercury were abolished or superimposed (respectively) by estrogenic replacement therapy (0.025 mg/kg 17beta estradiol cypionate, intramuscular). These effects were associated with a significant reduction in mercury content of the anterior pituitary gland and medial hypothalamus, suggesting a protective estrogenic effect.

The aim of the present study was to evaluate mercury and selenium concentrations in hair samples of reproductive age women from riverside communities of the Tapajós River basin. We studied 19 pregnant and 21 non-pregnant women, 13 to 45 years old, living in the region for at least 2 years, and having a diet rich in fish. The analysis of Se and total Hg were performed in the Instituto de Pesquisas Energéticas e Nucleares (IPEN, São Paulo, Brazil) by using a Varian AA220-FS atomic absorption spectrometer with a flow injection system. There were no differences between the two groups - pregnant and non-pregnant -- concerning age (23.80 +/- 6.92 and 26.60 +/- 9.60 years old, respectively) and residential time (20.21 +/- 8.30 and 22.20 +/- 10.90 years, respectively). The geometric means and ranges for total Hg concentration were similar (p > 0.05): 8.25 microg/g (1.51-19.43) in pregnant and 9.39 microg/g (5.25-21.00) in non-pregnant women, respectively. Total Hg concentrations were also similar in different gestational stages. However, there was a significant difference between the two groups (p < 0.05, Student t test) in relation to Se concentration: 0.61 microg/g (0.40-2.33) in pregnant and 2.46 microg/g (0.92-5.74) in non-pregnant women, respectively. We concluded that Hg exposure levels in reproductive age women were only slightly higher than a provisional tolerable weekly intake of MeHg would provide, that Hg concentration in maternal hair samples was independent of gestational age, and that low Se concentration in pregnant women indicates high mineral consumption by fetal organism to satisfy their metabolic requirements raised during pregnancy, including as a protective mechanism for Hg cytotoxic effects.

A quantitative study was conducted on the density of Langerhans cells (LCs) CD1a+ in specimens obtained from patients with American tegumentary leishmaniasis (ATL) lesions without previous treatment, as well as from control healthy individuals. LC density was significantly higher among infected patients when compared to controls and also higher in longer term ones. Regarding parasite quantities, these were proportionally inverse and diminished in chronic patients. Localized cutaneous leishmaniasis (LCL) showed an increase in cell population when compared to diffuse cutaneous leishmaniasis (DCL). A tendency towards density increase was observed in LC Leishmania (Leishmania) amazonensis patients when compared to Leishmania (Viannia) sp. Regarding the delayed hypersensitivity test (DTH, Montenegro skin test), L. (L.) amazonensis demonstrated a peculiar behavior because it is a poor cell immune inducer, presenting--among LCL patients--higher density in negative Montenegro patients than in positive ones. Negative DTH responses are usually poor in LC, although this was not evidenced in this study, possibly due to cell reposition, in order to stimulate immune response. Such results confirm the important role of LC in ATL, while suggesting that L. (L.) amazonensis may be a good model for LC studies as APC in ATL, due to its spectral immunological and clinical behavior.

The possible protective effects of glutathione (GSH), cysteine (CYS) and methionine (MET) on the Methylmercury (MeHg)-induced dopamine (DA) release from rat striatum were investigated using in vivo microdialysis coupled to HPLC with electrochemical detection. Intrastriatal infusion of MeHg 400 microM increased extracellular DA levels to 1941 +/- 199% in terms of basal levels. Infusion of MeHg 400 microM in GSH 400 microM pretreated animals, only increased striatal DA levels to 465 +/- 104%, in terms of basal levels, this increase being 76% lower than induced by MeHg alone. Conversely, the infusion of MeHg 400 microM after infusion of GSH 400 microM increased DA levels to 1019 +/- 96% in terms of basal levels, this increase being 47.5% lower than that observed in MeHg non-pretreated animals. The infusion of MeHg 400 microM in CYS 400 microM -pretreated animals, increased striatal DA levels to 740 +/- 149%, in terms of basal levels, this increase being 62% lower than that induced by MeHg in non-pretreated animals. The infusion of MeHg 400 microM in MET 400 microM pretreated animals increased striatal DA levels to 2011 +/- 230% in terms of basal, an increase that was not significantly different from that produced by MeHg 400 muM alone. In summary, the administration of compounds containing free -SH groups prevented the MeHg-induced DA release from rat striatum, probably due to the binding of MeHg to -SH groups. This would result in a lower metal availability to interact with -SH membrane proteins groups, which would decrease MeHg ability to interact with DA transporter.

The present study was carried out in order to determine the effects of intrastriatal administration of different doses (40 microM, 400 microM, and 4mM) of methylmercury (MeHg) on dopaminergic system of rat striatum. Experiments were performed in conscious and freely moving rats using brain microdialysis coupled with liquid chromatography. Intrastriatal administration of MeHg produced significant increases in dopamine (DA) striatal levels (907+/-7%, 1870+/-319%, and 7971+/-534% for the doses of 40, 400 microM, and 4mM, with respect to basal). The increase in DA levels was associated with significant decreases in extracellular levels of its main metabolites dihydroxyphenylacetic acid (DOPAC) and homovallinic acid (HVA) (65.0+/-3.0% and 52.2+/-1.3%, respectively) using the dose of 4mM MeHg, whereas nonsignificant changes in metabolite levels were observed with the doses of 40 and 400 microM MeHg. A second infusion of 4mM MeHg 24h after first infusion also produced a rise of DA levels, but this increase was very small as compared with that produced by first infusion (7971+/-534% versus 985+/-186%). This second infusion of 4mM MeHg also decreased DOPAC and HVA levels, but this decrease was not significant as compared with that observed after first infusion (65.0+/-3.0% and 52.2+/-1.3% versus 62.4+/-5.2% and 63.4+/-7.4%, respectively). We discuss these effects based on a stimulated DA release and/or a decreased DA intraneuronal degradation.

In the present study, the effects of intrastriatal administration of different concentrations (40 microM, 400 microM, and 4 mM) of inorganic mercury (HgCl(2)) on the dopaminergic system of rat striatum were evaluated, using a microdialysis technique coupled to liquid chromatography-electrochemical detection. In previous studies, we discussed the effects of organic mercury (MeHg) administration on the striatal dopaminergic system on the basis of changes in the release and metabolism of striatal dopamine (DA). In the present study it is demonstrated that intrastriatal administration of all concentrations of HgCl(2) produced significant increases in the output of DA (1240, 2500, and 2658% for the concentrations of 40 microM, 400 microM, and 4 mM HgCl(2), respectively) from rat striatal tissue, associated with significant decreases in striatal levels of its metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) with the concentrations of 400 microM and 4 mM HgCl(2) (74.4 and 3.4% for DOPAC and 71.0 and 50.6% for HVA, respectively), whereas no changes in metabolite levels were observed with the concentration of 40 microM HgCl(2). These effects are explained as a result of stimulated DA release and/or changed DA metabolism. The effects of intrastriatal administration of HgCl(2) were compared with those of MeHg on DA extracellular levels., (Copyright 2001 Academic Press.)

Mercury is a neurotoxic agent that produces different effects on the brain. In the present work, the effects of chronic doses of methyl mercury (MeHg) were studied on the dopaminergic system of the rat striatum, using microdialysis coupled to high-performance liquid chromatography in order to quantify the in vivo release of dopamine (DA) and its acidic metabolites DOPAC and HVA. The administration of an equivalent total dose of 6 mg/kg of MeHg induced significant increases in the striatal release of DA and/or its acidic metabolites, independently of the pattern of administration. These effects are discussed on the base of the release and the metabolization of DA. In conclusion, the effect of MeHg administered under these experimental conditions on the in vivo release of DA and its metabolites seems to have a dose-dependent component and seems to be an accumulative process., (Copyright 1997 Academic Press.)