[Show abstract][Hide abstract] ABSTRACT: Canine rangeliosis (popular names: “nambi-uvú”, i.e. bleeding ears; “peste de sangue”, i.e. bleeding plague; and “febre amarela dos cães”, i.e. yellow fever of dogs) is a tick-borne hemolytic and hemorrhagic disease caused by the protozoan parasite Rangelia vitalii which infects erythrocytes, leukocytes, and endothelial cells of blood capillaries. Rangelia vitalii was first reported as a novel piroplasm of dogs in 1910 in Brazil, a discovery that was met with skepticism at that time. Canine rangeliosis has been diagnosed in domestic dogs not only in Brazil but also in other South American countries (Argentina and Uruguay). Rangelia vitalii infection has also been found incidentally in Brazil in wild dogs (Cerdocyon thous, the crab-eating fox). Despite the fact that researchers in the early 1900s suggested that R. vitalii was a hitherto unidentified piroplasm that would be transmitted by the tick Amblyomma aureolatum, it was not until 2012 that these hypotheses were actually confirmed by PCR and transmission studies. Molecular studies have shown that R. vitalii is related to the Babesia sensu strictu clade, but genetically different from other morphologically similar species of Babesia that infect dogs. Another difference between Babesia spp. and R. vitalii is the ability of R. vitalii to invade endothelial cells, erythrocytes, and leukocytes. Experimental infection in dogs has successfully reproduced the clinical picture and pathology of the natural disease. In this article, epidemiology, clinical signs, laboratory findings, pathogenetic mechanisms including oxidative stress and immune response, necropsy findings, microscopic lesions, diagnosis, and treatment of canine rangeliosis are reviewed. What is currently known about this protozoal disease since its first report over a century ago is presented herein.
[Show abstract][Hide abstract] ABSTRACT: The present study investigated the effects of quercetin on the impairment of memory and anxiogenic - like behavior induced by cadmium (Cd) exposure. We also investigated possible alterations in acetylcholinesterase (AChE), Na(+),K(+)-ATPase and δ - aminolevulinate dehydratase (δ-ALA-D) activities as well as in oxidative stress parameters in the CNS. Rats were exposed to Cd (2.5mg/Kg) and quercetin (5, 25 or 50mg/Kg) by gavage for 45days. Animals were divided into eight groups (n=10-14): saline/control, saline/Querc 5mg/kg, saline/Querc 25mg/kg, saline/Querc 50mg/kg, Cd/ethanol, Cd/Querc 5mg/kg, Cd/Querc 25mg/kg and Cd/Querc 50mg/kg. Results demonstrated that Cd impaired memory and has anxiogenic effect.Quercetin prevented these harmful effects induced by Cd. AChE activity decreased in cerebral cortex and hippocampus and increased in hypothalamus of Cd-exposed rats. The Na(+),K(+)-ATPase activity decreased in cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin prevented these effects in AChE and Na(+),K(+)-ATPase activities. Reactive oxygen species production, thiobarbituric acid reactive substance levels, protein carbonyl content and double - stranded DNA fractions increased in cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin prevents totally or partially these effects caused by Cd. Total thiols (T-SH), reduced glutathione (GSH), reductase glutathione (GR) activities decreased and glutathione S-transferase (GST) activity increased Cd exposure rats. Co-treatment with quercetin prevented reduction in T-SH, GSH, GR activities and the rise of GST activity. The present findings show that quercetin prevents alterations in oxidative stress parameters as well as AChE and Na(+),K(+)-ATPase activities, consequently preventing memory impairment and anxiogenic-like behavior displayed by Cd exposure. These results may contribute to a better understanding of the neuroprotective role of quercetin, emphasizing the influence of this flavonoid in the diet for human health, possibly preventing brain injury associated with Cd intoxication.
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to investigate whether the flavonoid quercetin can prevent alterations in the behavioral tests and of cholinergic neurotransmission in rats submitted to the ethidium bromide (EB) experimental demyelination model during events of demyelination and remyelination.
Wistar rats were randomly distributed into four groups (20 animals per group): Control (pontine saline injection and treatment with ethanol), Querc (pontine saline injection and treatment with quercetin), EB (pontine 0.1% EB injection and treatment with ethanol), and EB+Querc (pontine 0.1% EB injection and treatment with quercetin). The groups Querc and Querc+EB were treated once daily with quercetin (50mg/kg) diluted in 25% ethanol solution (1ml/kg) and the animals of the control and EB groups were treated once daily with 25% ethanol solution (1ml/kg). Two stages were observed: phase of demyelination (peak on day 7) and phase of remyelination (peak on day 21 post-injection). Behavioral tests (beam walking, foot fault and inclined plane test), acetylcholinesterase (AChE) activity and lipid peroxidation in pons, cerebellum, hippocampus, hypothalamus, striatum and cerebral cortex were measured.
The quercetin promoted earlier locomotor recovery, suggesting that there was demyelination prevention or further remyelination velocity as well as it was able to prevent the inhibition of AChE activity and the increase of lipidic peroxidation, suggesting that this compound can protect cholinergic neurotransmission.
These results may contribute to a better understanding of the neuroprotective role of quercetin and the importance of an antioxidant diet in humans to provide benefits in neurodegenerative diseases such as MS.
Life sciences 04/2014; 103(2). DOI:10.1016/j.lfs.2014.03.033 · 2.70 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Scutia buxifolia is a native tree of Southern Brazil, Uruguay, and Argentina, which is popularly known as "coronilha" and it is used as a cardiotonic, antihypertensive and diuretic substance. The aim of this study was to assess the acute and sub-acute toxicity of the ethyl acetate fraction from the stem bark S. buxifolia in male and female mice.
The toxicity studies were based on the guidelines of the Organization for Economic Cooperation and Development (OECD-guidelines 423 and 407). In an acute study, a single dose of 2000mg/kg of S. buxifolia was administered orally to male and female mice. Mortality, behavioral changes, and biochemical and hematological parameters were evaluated. In the sub-acute study, S. buxifolia was administered orally to male and female mice at doses of 100, 200, and 400mg/kg/day for 28 days. Behavioral changes and biochemical, hematological, and histological analysis were evaluated.
The acute administration of S. buxifolia did not cause changes in behavior or mortality. Male and female mice presented decreased levels of platelets. Female mice presented decreased levels of leukocytes. On the other hand, in a sub-acute toxicity study, we observed no behavioral changes in male or female mice. Our results demonstrated a reduction in glucose levels in male mice treated to 200 and 400mg/kg of S. buxifolia. Aspartate aminotransferase (ASAT) activity was increased by S. buxifolia at 400mg/kg in male mice. In relation to the hematological parameters, male mice presented a reduction in hemoglobin (HGB) and hematocrit (HCT) when treated to 400mg/kg of plant fraction. Female mice showed no change in these parameters. Histopathological examination of liver tissue showed slight abnormalities that were consistent with the biochemical variations observed.
S. buxifolia, after acute administration, may be classified as safe (category 5), according to the OECD guide. However, the alterations observed, after sub-acute administration with high doses of ethyl acetate fraction from the stem bark S. buxifolia, suggest that repeated administration of this fraction plant can cause adverse hepatic, renal, and hematological effects.
Journal of ethnopharmacology 04/2014; 153(3). DOI:10.1016/j.jep.2014.03.063 · 3.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to assess whether α-tocopherol administration prevented alterations in the ectonucleotidase activities and platelet aggregation induced by high-fat diet in rats. Thus, we examined four groups of male rats which received standard diet, high-fat diet (HFD), α-tocopherol (α-Toc), and high-fat diet plus α-tocopherol. HFD was administered ad libitum and α-Toc by gavage using a dose of 50 mg/kg. After 3 months of treatment, animals were submitted to euthanasia, and blood samples were collected for biochemical assays. Results demonstrate that NTPDase, ectonucleotide pyrophosphatase/phosphodiesterase, and 5'-nucleotidase activities were significantly decreased in platelets of HFD group, while that adenosine deaminase (ADA) activity was significantly increased in this group in comparison to the other groups (P < 0.05). When rats that received HFD were treated with α-Toc, the activities of these enzymes were similar to the control, but ADA activity was significantly increased in relation to the control and α-Toc group (P < 0.05). HFD group showed an increased in platelet aggregation in comparison to the other groups, and treatment with α-Toc significantly reduced platelet aggregation in this group. These findings demonstrated that HFD alters platelet aggregation and purinergic signaling in the platelets and that treatment with α-Toc was capable of modulating the adenine nucleotide hydrolysis in this experimental condition.
Journal of physiology and biochemistry 03/2014; 70(2). DOI:10.1007/s13105-014-0327-2 · 1.97 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of this paper was to report a case of a female Rottweiler dog, 9 years old, presenting eccentrocytes in blood caused by the presence of a lipoma. This morphological change in red blood cells is considered uncommon, especially when related to cancer. The blood count revealed the presence of eccentrocytes, while the fine-needle aspiration cytology and histopathology of the nodule revealed to be a lipoma. Pre-surgical tests showed high levels of lipid peroxidation in the bloodstream, a parameter for assessment of oxidative stress, and increased antioxidant enzymes. Ten days after removal of the neoplasm, the values of lipid peroxidation and antioxidant enzymes decreased. One month after the surgery, there were no eccentrocytes in blood circulation. Thus, it appears that the occurrence of eccentrocytes in this case is linked to the presence of lipoma, which leads to an increase in lipid peroxidation and in antioxidant enzymes activities.
[Show abstract][Hide abstract] ABSTRACT: Anthocyanins are a group of natural phenolic compounds responsible for the colour to plants and fruits. These compounds might have beneficial effects on memory and have antioxidant properties. In the present study we have investigated the therapeutic efficacy of anthocyanins in an animal model of cognitive deficits, associated to Alzheimer's disease, induced by scopolamine. We evaluated whether anthocyanins protect the effects caused by SCO on nitrite/nitrate (NOx) levels and Na(+),K(+)-ATPase and Ca(2+)-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex and hippocampus (of rats. We used 4 different groups of animals: control (CTRL), anthocyanins treated (ANT), scopolamine-challenged (SCO), and scopolamine+anthocyanins (SCO+ANT). After seven days of treatment with ANT (200mg/kg; oral), the animals were SCO injected (1mg/kg; IP) and were performed the behavior tests, and submitted to euthanasia. A memory deficit was found in SCO group, but ANT treatment prevented this impairment of memory (P<0.05). The ANT treatment per se had an anxiolitic effect. AChE activity was increased in both in cortex and hipoccampus of SCO group, this effect was significantly attenuated by ANT (P<0.05). SCO decreased Na(+),K(+)-ATPase and Ca(2+)-ATPase activities in hippocampus, and ANT was able to significantly (P<0.05) prevent these effects. No significant alteration was found on NOx levels among the groups. In conclusion, the ANT is able to regulate cholinergic neurotransmission and restore the Na(+),K(+)-ATPase and Ca(2+)-ATPase activities, and also prevented memory deficits caused by scopolamine administration.
International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience 12/2013; 33(1). DOI:10.1016/j.ijdevneu.2013.12.006 · 2.58 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to analyze if the pre-administration of anthocyanin on memory and anxiety prevented the effects caused by intraceberoventicular streptozotocin (icv-STZ) administration-induced sporadic dementia of Alzheimer's type (SDAT) in rats. Moreover, we evaluated whether the levels of nitrite/nitrate (NOx), Na(+),K(+)-ATPase, Ca(2+)-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex (CC) and hippocampus (HC) are altered in this experimental SDAT.
Male Wistar rats were divided in 4 different groups: control (CTRL), anthocyanin (ANT), streptozotocin (STZ) and streptozotocin+anthocyanin (STZ+ANT). After seven days of treatment with ANT (200mg/kg; oral), the rats were icv-STZ injected (3mg/kg), and four days later were performed the behavior parameters and submitted to euthanasia.
A memory deficit was found in STZ group, but ANT treatment showed to prevent this impairment of memory (P<0.05). Our results showed a higher anxiety in icv-STZ group, but the treatment with ANT showed a per se effect and prevented the anxiogenic behavior induced by STZ. Our results reveal that ANT (100μM) tested diplace the specific binding of [H(3)] flunitrazepam to benzodiazepinic site of GABAA receptors. AChE, Ca(+)-ATPase activities and NOx levels were found to be increased in HC and CC in STZ group, which was attenuated by ANT (P<0.05). STZ decreased Na(+),K(+)-ATPase activity and ANT was able to prevent these effects (P<0.05).
In conclusion, these findings demonstrated that ANT is able to regulate ions pump activity and cholinergic neurotransmission, as well as able to enhance memory and act as anxiolytic compound in animals with SDAT.
Life sciences 11/2013; 96(1-2). DOI:10.1016/j.lfs.2013.11.014 · 2.70 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This study evaluated the effects of curcumin and/or insulin on antioxidant enzyme activity in blood, liver, and kidney, as well as on lipid peroxidation and delta aminolevulinic dehydratase (δ-ALA-D) activity, and a histopathological analysis of streptozotocin-induced diabetic rats. The animals were divided into six groups (n = 6): control/saline (C); control/curcumin (CCur); diabetic/saline (D); diabetic/insulin (DIns); diabetic/curcumin (DCur); and diabetic/insulin/curcumin (DInsCur). After 30 days of treatment with curcumin and/or insulin, the animals were sacrificed and the liver, kidney, and serum were used for experimental determinations. Results of histopathological analysis showed that the treatment with insulin ameliorate renal and hepatic lesions from both DIns and DInsCur groups. TBARS levels were significantly increased in serum, liver, and kidney in D group and the administration of curcumin and insulin prevented this increase in DIns and DCur groups. The activities of catalase (CAT), superoxide dismutase, and δ-ALA-D presented a significant decrease in the liver and kidney D group when compared to C group (P < 0.05). The animals treated with curcumin and insulin presented an increase of CAT activity, revealing a positive interaction between both substances. The treatments with curcumin or insulin prevented oxidative stress in blood, through modulation of enzymatic antioxidant defenses. These findings contributed to the comprehension that antioxidants from medicinal plants could be used as adjuvant in the treatment of this endocrinopathy and not as single therapy.
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to investigate neurochemical and enzymatic changes in rats infected with Trypanosoma evansi, and their interference in the cognitive parameters. Behavioural assessment (assessment of cognitive performance), evaluation of cerebral L-[3H]glutamate uptake, acetylcholinesterase (AChE) activity and Ca+2 and Na+, K+-ATPase activity were evaluated at 5 and 30 days post infection (dpi). This study demonstrates a cognitive impairment in rats infected with T. evansi. At 5 dpi memory deficit was demonstrated by an inhibitory avoidance test. With the chronicity of the disease (30 dpi) animals showed anxiety symptoms. It is possible the inhibition of cerebral Na+, K+-ATPase activity, AChE and synaptosomal glutamate uptake are involved in cognitive impairment in infected rats by T. evansi. The understanding of cerebral host–parasite relationship may shed some light on the cryptic symptoms of animals and possibly human infection where patients often present with other central nervous system (CNS) disorders.
[Show abstract][Hide abstract] ABSTRACT: This study investigated the effect of quercetin on nucleoside triphosphate diphosphohydrolase (NTPDase), 5'-nucleotidase, adenosine deaminase (ADA), and acetylcholinesterase (AChE) activities in synaptosomes from cerebral cortex of adult rats exposed to cadmium (Cd). Rats were exposed to Cd (2.5 mg/Kg) and quercetin (5, 25 or 50 mg/Kg) by gavage for 45 days. Rats were randomly divided into eight groups (n = 8-10): saline/ethanol, saline/Querc 5 mg/kg, saline/Querc 25 mg/kg, saline/Querc 50 mg/kg, Cd/ethanol, Cd/Querc 5 mg/kg, Cd/Querc 25 mg/kg, and Cd/Querc 50 mg/kg. Results demonstrated that AChE activity increased in the Cd/ethanol group when compared to saline/ethanol group. Treatment with quercetin prevented the increase in AChE activity when compared to Cd/ethanol group. Quercetin treatment prevented the cadmium-induced increase in NTPDase, 5-nucleotidase, and ADA activities in Cd/ethanol group when compared to saline/ethanol group. Our data showed that quercetin have a protector effect against Cd intoxication. This way, is a promising candidate among the flavonoids to be investigated as a therapeutic agent to attenuate neurological disorders associated with Cd intoxication.
[Show abstract][Hide abstract] ABSTRACT: Rangelia vitalii is a tick-transmitted piroplasm that causes both hemolytic and hemorrhagic disease in dogs in Brazil.
The aim of this study was to evaluate the response of the bone marrow in dogs experimentally infected with R vitalii during the acute stage of the disease.
For this study, 2 groups of a total of 12 young dogs were used. Group A was composed of healthy dogs (n = 5), and group B consisted of animals infected with R vitalii (n = 7). Blood samples were collected on days 0, 10, 20, and 30 post-inoculation and stored in EDTA tubes for a full hematology profile, including a reticulocyte count. On days 10 and 20, bone marrow samples were collected, stained, and examined.
In infected dogs anemia was identified on days 10 and 20 post-inoculation (P < .01), and on day 20 reticulocytosis was present. Infected dogs had leukopenia due to neutropenia and eosinopenia, along with lymphocytosis and monocytosis, when compared with control animals. In bone marrow, the myeloid:erythroid ratio was significantly decreased (P < .05) in infected dogs due to increased erythroid precursors.
Dogs experimentally infected with R vitalii develop regenerative extravascular hemolytic anemia accompanied by erythroid hyperplasia in the bone marrow. During the acute phase of the disease, leukopenia due to neutropenia and eosinopenia suggests intense tissue recruitment of these cells in response to the endothelial damage caused by this parasite.
[Show abstract][Hide abstract] ABSTRACT: The purpose of the present investigation was to evaluate the hydrolysis of adenine nucleotides on synaptosomes and platelets obtained from rats exposed to cadmium (Cd) and treated with N-acetylcysteine (NAC). Rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 4–6): control/saline, NAC, Cd, and Cd/NAC. The results of this study demonstrated that NTPDase and 5′-nucleotidase activities were increased in the cerebral cortex synaptosomes of Cd-poisoned rats, and NAC co-treatment reversed these activities to the control levels. In relation to hippocampus synaptosomes, no differences on the NTPDase and 5′-nucleotidase activities of Cd-poisoned rats were observed and only the 5′-nucleotidase activity was increased by the administration of NAC per se. In platelets, Cd-intoxicated rats showed a decreased NTPDase activity and no difference in the 5′-nucleotidase activity; NAC co-treatment was inefficient in counteracting this undesirable effect. Our findings reveal that adenine nucleotide hydrolysis in synaptosomes and platelets of rats were altered after Cd exposure leading to a compensatory response in the central nervous system and acting as a modulator of the platelet activity. NAC was able to modulate the purinergic system which is interesting since the regulation of these enzymes could have potential therapeutic importance. Thus, our results reinforce the importance of the study of the ecto-nucleotidases pathway in poisoning conditions and highlight the possibility of using antioxidants such as NAC as adjuvant against toxicological conditions.
International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience 02/2013; 31(1):69–74. DOI:10.1016/j.ijdevneu.2012.11.001 · 2.58 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: production of a free radical formation, with high production of the reactive oxygen species (ROS) that has been attributed to protein glycation and/or glucose auto-oxidation, due to a hyperglycemic environment. Increased oxidative stress may be the result of a pathological process. [1-3] Literature describes that ROS plays a role in a variety of physiological and pathophysiological processes of diabetes such as nephropathy  and non-alcoholic fatty liver disease. [4,5] Therefore, this disease has shown an increase in the renal and hepatic function biomarkers. [1,5,6] Another common effect in diabetes is the high activity INTRODUCTION
Journal of Pharmaceutical Negative Results 01/2013; 4(1):5-12. DOI:10.4103/0976‑9234.116755
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to evaluate biochemical parameters of iron metabolism in rats experimentally infected with T. evansi. To this end, 20 rats (Wistar) were intraperitoneally inoculated with blood containing trypomastigotes 10(6) (Group T) and 12 animals were used as negative control (Group C) and received saline (0.2 mL) through same route. Blood samples were collected by cardiac puncture on day 5 (C5, T5) and 30 (C30, T30) post-inoculation (pi) to perform complete blood count and determination of serum iron, transferrin, ferritin, total and latent iron fixation capacity, transferrin saturation and prohepcidin concentration. Also, bone marrow samples were collected, to perform Pearls staining reaction. Levels of iron, total and latent iron binding capacity and prohepcidin concentration were lower (P <0.05) in infected rats (T5 and T30 groups) compared to controls. On the other hand, levels of transferrin and ferritin were higher when compared to controls (P <0.05). The transferrin saturation increased on day 5 pi, but decreased on day 30 pi. The Pearls reaction showed a higher accumulation of iron in the bone marrow of infected animals in day 5 pi (P <0.01). Infection with T. evansi in rats caused anemia and changes in iron metabolism associated to the peaks of parasitemia. These results suggest that changes in iron metabolism may be related to the host immune response to infection and anemic status of infected animals.
[Show abstract][Hide abstract] ABSTRACT: The potent activity against Trypanosomes and health beneficial effects of curcumin (Cur) has been demonstrated in various experimental models. In this study, we evaluated the in vivo effect of Cur as trypanocide and as potential anti-inflammatory agent, through the evaluation of immunomodulatory mechanisms in rats infected with Trypanosoma evansi. Daily oral Cur was administered at doses of 0, 20 or 60 mg/kg as preventive treatment (30 and 15 days pre infection) and as treatment (post infection). The treatment of the groups continued until the day of euthanasia. Fifteen days after inoculation, parasitemia, plasma proinflammatory cytokines (IFN-γ, TNF-α, IL-1, IL-6), anti-inflammatory cytokines (IL-10) and blood acetylcholinesterase activity (AChE) were analyzed. Pretreatment with Cur reduced parasitemia and lethality. Cur inhibited AChE activity and improved immunological response by cytokines proinflammatory, fundamental during T. evansi infection. We found that Cur is not so important as an antitrypanosomal activity but as immunomodulator agent. These findings reveal that the preventive use of Cur stimulates anti-inflammatory mechanisms, reducing an excessive inflammatory response.
Parasitology International 11/2012; 62(2). DOI:10.1016/j.parint.2012.11.004 · 1.86 Impact Factor