Hippocampal acetylcholinesterase activation induced by streptozotocin in mice is protected by an organotellurium compound without evidence of toxicity.

The cognitive deficit, which is like Alzheimer's disease and is associated with oxidative damage, may be induced by exposure to streptozotocin. This study aimed to evaluate if the tellurium-containing organocompound, 3j, 5'-arylchalcogeno-3-aminothymidine derivative, interferes with the effects of streptozotocin, as well as to investigate its toxicity in adult mice. Cognitive deficit was induced by two doses of streptozotocin (2.25 mg/kg/day, 48 h interval) intracerebroventricularly. After, the mice were subcutaneously treated with 3j (8.62 mg/kg/day) for 25 days. The effects were assessed by evaluating hippocampal and cortical acetylcholinesterase and behavioral tasks. 3j toxicity was investigated for 10 (0, 21.55, or 43.10 mg/kg/day) and 37 (0, 4.31, or 8.62 mg/kg/day) days by assessing biometric parameters and glucose and urea levels, and alanine aminotransferase activity in blood plasma. 3j exposure did not alter the behavioral alterations induced by streptozotocin exposure. On the other hand, 3j exposure normalized hippocampus acetylcholinesterase activity, which is enhanced by streptozotocin exposure. Toxicity evaluation showed that the administration of 3j for either 10 or 37 days did not cause harmful effects on the biometric and biochemical parameters analyzed. Therefore, 3j does not present any apparent toxicity and reverts acetylcholinesterase activity increase induced by streptozotocin in young adult mice.

Mercury toxicity in pregnant and lactating rats: zinc and N-acetylcysteine as alternative of prevention.

This study evaluated the toxic effects of inorganic mercury (Hg) in pregnant and lactating rats, as well as the possible protective effect of zinc (Zn) and N-acetylcysteine (NAC). Pregnant and lactating rats were pre-treated with ZnCl2 (27 mg/kg) and/or NAC (5 mg/kg) and after 24 h, they were exposed to HgCl2 (10 mg/kg). Animals were sacrificed 24 h after Hg exposure, and biochemical tests and metal determination were performed. Regarding pregnant rats, Hg exposure caused kidney, blood, and placenta δ-aminolevulinic acid dehydratase (δ-ALA-D) activity inhibition, and the pre-treatments showed a tendency of protection. Moreover, all the animals exposed to Hg presented high Hg levels in the kidney, liver, and placenta when compared with control group. Pregnant rats pre-exposed to Zn (Zn-Hg and Zn/NAC-Hg groups) presented an increase in hepatic metallothionein levels. Therefore, lactating rats exposed to Hg presented renal and blood δ-ALA-D inhibition; the pre-treatments showed a tendency to prevent the renal δ-ALA-D inhibition and prevented the blood δ-ALA-D inhibition caused by Hg. Lactating rats exposed to Hg presented high Hg levels in the kidney and liver. These results showed that 10 mg/kg of HgCl2 causes biochemistry alterations in pregnant and lactating rats, and Zn and NAC present promising results against these damages.

Combined platelet-rich plasma and cold water immersion treatment minimize the damage following a skeletal muscle stretch injury in rats.

The skeletal muscle stretch injuries are commonly observed in sports. In order to stimulate tissue healing, the platelet-rich plasma (PRP) and cold water immersion (CWI) are widely used in clinical practice. This study investigated the effects of isolated or combined PRP and/or CWI on the oxidative damage determined by a stretch injury induced in gastrocnemius muscle of rats. PRP and CWI are applied immediately after the injury, and the biochemical analysis was performed after 1, 3, 5, or 7 days. The levels of o thiobarbituric acid reactive substances and oxidized dichlorofluorescein were significantly increased, both in skeletal muscle tissue and erythrocytes preparations, and the combined PRP and CWI minimized these parameters. Moreover, combined PRP and CWI were more effective than the isolated treatments to increase catalase activity, also the ratio of reduced/oxidized glutathione, and the non-protein thiols (-SH) group levels. In conclusion, we could infer that the combination of these regular treatments used in an isolated form shows a great potential for treatments of muscular injuries.

Protection of cholinergic and antioxidant system contributes to the effect of Vitamin D3 ameliorating memory dysfunction in sporadic dementia of Alzheimer's type.

OBJECTIVE: Investigate Vitamin D3 (VD3) effect on the Acetylcholinesterase (AChE), oxidative damage and behavioral tests in animals subjected to Intracerebroventicular injection of Streptozotocin (ICV-STZ) simulating a Sporadic Dementia of Alzheimer's Type (SDAT) and treated with VD3 (21 days). METHODS: Animals were divided into eight groups: Vehicle, VD12.5 µg/kg, VD42 µg/kg, VD125 µg/kg, STZ, STZ+VD12.5 µg/kg, STZ+VD42 µg/kg, STZ+VD125 µg/kg. RESULTS: VD3 prevented the increase in AChE in groups of VD42 µg/kg and VD125 µg/kg; in AChE of synaptossomes and TBARS levels prevented the increase in group VD125 µg/kg; in ROS levels there was not a significant difference; for the Carbonyl Content all doses prevented the increase. Total Thiols prevent the decrease in VD42 µg/kg and VD125 µg/kg, and Reduced Glutathione prevented the decrease in VD125 µg/kg, Oxidized Glutathione prevented the increase in VD125 µg/kg. In relation to behavioral tests, the VD3 prevented the increase in time to find (days 2 and 3), in the time to find the platform (day 3) and in time spent in the quadrant (day 2). However, in relation to crossings there was not difference in groups. These results indicated the therapeutic effect of the VD3 in model of STZ in rats.

The bioaccumulation of waterborne zinc in tissues of silver catfish (Rhamdia quelen) and its effect on biochemical parameters.

Silver catfish (Rhamdia quelen) is a fish species with neotropical distribution, and is a potential model organism to study polluted environment. The aim of this study is to analyze the response of silver catfish to environmental concentrations of waterborne zinc (Zn) over 96 h. Significant metal accumulation was seen in gill, intestine and liver tissues. No significant accumulation was seen in muscle tissue. Lipid peroxidation increased in the brain, and decreased in the muscle and liver at all levels of exposure. Zinc exposure led to decreased protein carbonyl levels in the brain and increased levels in the liver. The activity of catalase in the liver was reduced for all exposed groups. Glutathione S-transferase activity decreased in the brain at the highest level of exposure and in the liver at all Zn concentrations tested. Non-protein thiols increased in the muscle and in the gills after exposure. Ascorbic acid levels increased in the brain and in the gills. Exposure to Zn also altered the metabolic parameters, causing decreased lactate and ammonia levels in the muscle, and decreased glycogen in the liver. Zinc exposure increased ammonia and amino acid levels in the liver, and increase glycogen and amino acid levels in muscle tissue. Our results demonstrate that exposure to environmentally relevant concentrations of Zn led to accumulation of metals in the tissues of silver catfish, with significant changes in biochemical parameters.

Effects of diphenyl diselenide diet on a model of mercury poisoning.

This work investigated the preventive effect of diphenyl diselenide [(PhSe)2] against the toxic effects of mercury in silver catfish (Rhamdia quelen). The animals were treated during 30 consecutive days with a (PhSe)2 supplemented feed (3.0 mg kg-1) or commercial feed. During the last 5 days the animals received a daily intraperitoneal dose of HgCl2 (1.7 mg kg-1) or Saline (0.9%). Twenty-four hours after the last HgCl2 injection, the animals were euthanized by spinal cord section to biological material obtainment. Hepatic (AST and ALT) and renal (ammonia and creatinine) toxicity biomarkers, δ-ALA-D activity, TBARS, total and non-protein thiols levels and hepatic, renal and blood mercury (Hg) and zinc (Zn) content were evaluated. Considering renal parameters, HgCl2 exposition increased serum creatinine levels and decreased δ-ALA-D activity, total and non-protein thiols and TBARS levels. HgCl2 exposure also decreased blood δ-ALA-D activity. With exception of blood δ-ALA-D activity and total thiols levels, (PhSe)2 supplementation partially prevented mercury induced alterations. Animals exposed to HgCl2 presented an increase in liver and kidney Hg content and a decrease in liver and blood Zn content. The alteration in blood Zn content was partially prevented with (PhSe)2 supplementation. With the exception of mercury and zinc content, no effects of HgCl2 exposure on hepatic tissue were observed. These results show that (PhSe)2 supplementation can represent a promising alternative to prevent the toxic effects presented by Hg exposure.

Selenothymidine protects against biochemical and behavioral alterations induced by ICV-STZ model of dementia in mice.

The present study evaluated the neuroprotective effects of one selenium-containing AZT derivative compound (S1073) in memory and learning impairment caused by Intracerebroventricular-streptozotocin (ICV-STZ). ICV-STZ in mice causes impairment of energy metabolism with oxidative damage and cholinergic dysfunction, and provides a relevant model for sporadic dementia of Alzheimer's type (AD). Acetylcolinesterase (AChE), Catalase (CAT), dichlorofluorescein oxidation (DCFH), TBARS and thiol content were measured. Swiss adult mice were pre-treated with S1073 [1 mmol/kg] (i.p.) and after 30 min of the injection received a bilateral dose of STZ [11.3 µmol/l]. After 8 days' STZ injection, we performed the behavioral experiments (Beaker test, Open field and Morris water maze task). ICV-STZ caused significant learning and memory impairments, which were significantly improved by S1073 pre-treatment. A significant increase in cerebral DFCH, TBARS levels and AChE activity and a disturbance in the memory and learning were observed in ICV-STZ injected animals. S1073 significantly ameliorated all alterations induced by ICV-STZ in mice. All these findings support the neuroprotective role of S1073 in mice model of Alzheimer's dementia-type induced by ICV-STZ, which may be associated with its antioxidant activity and/or with its inhibitory effect in brain AChE. In fact, in silico analysis indicated that S1073 may be an inhibitor of AChE.

Copper attenuates early and late biochemical alterations induced by inorganic mercury in young rats.

Mercury (Hg), a divalent metal, produces adverse effects predominantly in the renal and central nervous systems. The aim of this study was to determine the effectiveness of copper (Cu) in prevention of mercuric mercury (Hg2+)-mediated toxic effects as well as the role metallothioneins (MT) play in this protective mechanism in young rats. Wistar rats were treated subcutaneously with saline (Sal) or CuCl2.2H2O (Cu 2.6 mg/kg/day) from 3 to 7 days old and with saline or HgCl2 (Hg 3.7 mg/kg/day) from 8 to 12 days old. The experimental groups were (1) Sal-Sal, (2) Cu-Sal, (3) Sal-Hg, and (4) Cu-Hg. MTs and metal contents were determined at 13 and 33 days of age. Porphobilinogen synthase (PBG-synthase) activity as well as renal and hepatic parameters were measured at 33 days. At 13 day, Hg2+ exposure increased hepatic MT, Hg, zinc (Zn) and iron (Fe) levels, in kidney elevated Cu and Hg and decreased renal Fe concentrations, accompanied by elevated blood Hg levels. At 33 days, Hg2+ exposure inhibited renal PBG-synthase activity, increased serum urea levels and lowered Fe and Mg levels. Copper partially prevented the rise in blood Hg and liver Fe noted at 13 days; and completely blocked urea rise and diminished renal PBG-synthase activity inhibition at 33 days. In 13-day-old rats, Cu exposure redistributed the Hg in the body, decreasing hepatic and blood levels while increasing renal levels, accompanied by elevated renal and hepatic MT levels in Hg2+-exposed animals. These results suggest that hepatic MT might bind to hepatic and blood Hg for transport to the kidney in order to be excreted. ABBREVIATIONS: MT: metallothioneins; PBG-synthase: porphobilinogen synthase.

Associação Entre Força Muscular Relativa e Risco Cardiometabólico em Pacientes Hipertensos / Association between Relative Muscular Strength and Cardiometabolic Risk in Hypertensive Patients

Introdução: A força muscular tem sido considerada bom preditor de risco para doenças cardiovasculares. Objetivo: Avaliar a associação entre força muscular relativa com fatores de risco cardiometabólicos em pacientes hipertensos. Métodos: Estudo transversal realizado com 115 pacientes hipertensos atendidos em um hospital universitário. Foram coletadas variáveis antropométricas e bioquímicas (glicemia de jejum, colesterol total e frações e triglicerídeos). Foram calculados os indicadores razão cintura/altura e Índice de massa corporal. A força muscular relativa foi avaliada a partir da força de preensão palmar, medida pelo dinamômetro, e dividida pelo peso corporal. A correlação de Pearson e o modelo de regressão linear foram utilizados para estimar a relação entre as variáveis de risco e a força muscular relativa. Foram adotados um nível de significância de 5% e intervalo de confiança de 95%. Resultados: A maioria da população (82,6%) foi do sexo feminino, 64,3% adultos, 56,5% sedentários e 93,0% com excesso de peso. Foram observadas correlações inversas significantes entre a força muscular relativa com a razão cintura/ altura e Índice de massa corporal (p=0,000). O modelo de regressão mostrou que o aumento na razão cintura/altura contribuiu significativamente para a redução da força de preensão palmar relativa (p=0,023), assim como ser do sexo feminino (p=0,000). Conclusão: O presente estudo identificou associação entre a força de preensão palmar relativa e variáveis de risco cardiometabólico

Introduction: Muscle strength has been considered a good predictor of risk for cardiovascular diseases. Objective: To evaluate the association between relative muscular strength and cardiometabolic risk factors in hypertensive patients. Methods: A cross-sectional study was carried out with 115 hypertensive patients attended at a university hospital. Anthropometric and biochemical variables (fasting glycemia, total cholesterol and fractions and triglycerides) were collected. The Waist / height ratio and body mass index were calculated. Relative muscle strength was assessed from the palmar grip strength, measured by the dynamometer, and divided by body weight. Pearson's correlation was used and the linear regression model to estimate the relationship between risk variables and relative muscle strength. A significance level of 5% and a 95% confidence interval were adopted. Results: The majority of the population (82.6%) were female, 64.3% were adults, 56.5% were sedentary and 93.0% were overweight. Significant inverse correlations were observed between relative muscle strength with waist / height ratio and body mass index (p=0.000). The regression model showed that the increase in waist / height ratio contributed significantly to the reduction of relative muscle strength (p = 0.023), as well as being female (p = 0.000). Conclusion: The present study identified an association between relative muscle strength and cardiometabolic risk variables

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Effects of Zinc and N-Acetylcysteine in Damage Caused by Lead Exposure in Young Rats.

This study investigated the toxicity of rats exposed to lead acetate (AcPb) during the second phase of brain development (8-12 days postnatal) in hematological and cerebral parameters. Moreover, the preventive effect of zinc chloride (ZnCl2) and N-acetylcysteine (NAC) was investigated. Pups were injected subcutaneously with saline (0.9% NaCl solution), ZnCl2 (27 mg/kg/day), NAC (5 mg/kg/day) or ZnCl2 plus NAC for 5 days (3rd-7th postnatal days), and with saline (0.9% NaCl solution) or AcPb (7 mg/kg/day) in the five subsequent days (8th-12th postnatal days). Animals were sacrificed 21 days after the last AcPb exposure. Pups exposed to AcPb presented inhibition of blood porphobilinogen-synthase (PBG-synthase) activity without changes in hemoglobin content. ZnCl2 pre-exposure partially prevented PBG-synthase inhibition. Regarding neurotoxicity biomarkers, animals exposed to AcPb presented a decrease in cerebrum acetylcholinesterase (AChE) activity and an increase in Pb accumulation in blood and cerebrum. These changes were prevented by pre-treatment with ZnCl2, NAC, and ZnCl2 plus NAC. AcPb exposure caused no alteration in behavioral tasks. In short, results show that AcPb inhibited the activity of two important enzymatic biomarkers up to 21 days after the end of the exposure. Moreover, ZnCl2 and NAC prevented the alterations induced by AcPb.

Acute mercury exposition of virgin, pregnant, and lactating rats: Histopathological kidney and liver evaluations.

This work investigated the effects of mercury chloride (HgCl2 ) acute exposure on virgin, pregnant and lactating rats by determination of renal and hepatic morphological and ultrastructural parameters and the expression of oxidative stress and stress tolerance markers, due to kidney and liver are the organs that more accumulate inorganic mercury. Adult Wistar rats virgin (90 days old), pregnant (18th gestation day) and lactating (7th lactation day) were injected once with HgCl2 (5 mg/kg) or saline (controls). We observed that HgCl2 exposure of virgin rats caused significant inflammatory infiltration and severe morphological variations, like glomeruli atrophy, dilatation of Bowman's capsule, tubular degeneration and hepatocytes alteration. Moreover, virgin rats presented mitochondrial modification, important oxidative stress and increase in stress tolerance proteins at both kidney and liver level, compared with virgin controls. In detail, virgin rats exposed to HgCl2 presented significantly elevated level of inducible nitric oxide synthase, heat shock protein 27 and glucose regulated proteins 75 expressions at both renal tubular and hepatocytes level, respect untreated virgin rats. Interestingly, pregnant and lactating rats exposed to HgCl2 presented weak renal and liver morphological alterations, showing weak inflammatory infiltration and no significant difference in structural mitochondrial transmembrane protein, oxidative stress markers and stress tolerance proteins expressions respect controls (virgin, pregnant and lactating rats). Although, both control and HgCl2 -exposed pregnant and lactating rats showed renal glomeruli greater in diameter respect virgin rats. In conclusion, we believe that virgin rats are more sensitive to HgCl2 toxicity respect pregnant and lactating rats. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1500-1512, 2017.

Effects of zinc against mercury toxicity in female rats 12 and 48 hours after HgCl2 exposure.

This work investigated the toxicity of inorganic mercury and zinc preventive effects in female rats sacrificed 12 or 48 h after HgCl2 exposure. Female Wistar rats were subcutaneously injected with ZnCl2 (27 mg/kg) or saline (0.9 %), and 24 h later they were exposed to HgCl2 (5 mg/kg) or saline (0.9 %). Rats sacrificed 12 hours after Hg administration presented an increase in kidney weight and a decrease in renal ascorbic acid levels. Zinc pretreatment prevented the renal weight increase. Rats sacrificed 48 h after Hg exposure presented a decrease in body weight gain, an increase in renal weight, a decrease in renal δ-aminolevulinic acid dehydratase activity, an increase in serum creatinine and urea levels, and a decrease in kidney total thiol levels. Zinc pretreatment partly prevented the decrease in body weight gain and increase in creatinine levels, in addition to totally preventing renal δ-aminolevulinic acid dehydratase inhibition. Mercury accumulation in the kidney and liver in both periods was observed after Hg administration. These results show the different Hg effects along the time of intoxication, and a considerably preventive effect of zinc against Hg toxicity.

Free radical scavenging in vitro and biological activity of diphenyl diselenide-loaded nanocapsules: DPDS-NCS antioxidant and toxicological effects.

Selenium compounds, such as diphenyl diselenide (DPDS), have been shown to exhibit biological activity, including antioxidant effects. However, the use of DPDS in pharmacology is limited due to in vivo pro-oxidative effects. In addition, studies have shown that DPDS-loaded nanocapsules (DPDS-NCS) have greater bioavailability than free DPDS in mice. Accordingly, the aim of this study was to investigate the antioxidant properties of DPDS-NCS in vitro and biological activity in mice. Our in vitro results suggested that DPDS-NCS significantly reduced the production of reactive oxygen species and Fe(II)-induced lipid peroxidation (LPO) in brain. The administration of DPDS-NCS did not result in death or change the levels of endogenous reduced or oxidized glutathione after 72 hours of exposure. Moreover, ex vivo assays demonstrated that DPDS-NCS significantly decreased the LPO and reactive oxygen species levels in the brain. In addition, the highest dose of DPDS-NCS significantly reduced Fe(II)- and sodium nitroprusside-induced LPO in the brain and Fe(II)-induced LPO in the liver. Also, δ-aminolevulinate acid dehydratase within the brain was inhibited only in the highest dose of DPDS-NCS. In conclusion, our data demonstrated that DPDS-NCS exhibited low toxicity in mice and have significant antioxidant characteristics, indicating that nanoencapsulation is a safer method of DPDS administration.

Zinc and N-acetylcysteine modify mercury distribution and promote increase in hepatic metallothionein levels.

This study investigated the ability of zinc (Zn) and N-acetylcysteine (NAC) in preventing the biochemical alterations caused by mercury (Hg) and the retention of this metal in different organs. Adult female rats received ZnCl2 (27mg/kg) and/or NAC (5mg/kg) or saline (0.9%) subcutaneously and after 24h they received HgCl2 (5mg/kg) or saline (0.9%). Twenty-four hours after, they were sacrificed and analyses were performed. Hg inhibited hepatic, renal, and blood δ-aminolevulinic acid dehydratase (δ-ALA-D) activity, decreased renal total thiol levels, as well as increased serum creatinine and urea levels and aspartate aminotransferase activity. HgCl2-exposed groups presented an important retention of Hg in all the tissues analyzed. All pre-treatments demonstrated tendency in preventing hepatic δ-ALA-D inhibition, whereas only ZnCl2 showed this effect on blood enzyme. Moreover, the combination of these compounds completely prevented liver and blood Hg retention. The exposure to Zn and Hg increased hepatic metallothionein levels. These results show that Zn and NAC presented promising effects against the toxicity caused by HgCl2.

Effectiveness of (PhSe)2 in protect against the HgCl2 toxicity.

This work investigated the preventive effect of diphenyl diselenide [(PhSe)2] on renal and hepatic toxicity biomarkers and oxidative parameters in adult mice exposed to mercury chloride (HgCl2). Selenium (Se) and mercury (Hg) determination was also carried out. Mice received a daily oral dose of (PhSe)2 (5.0mg/kg/day) or canola oil for five consecutive days. During the following five days, the animals were treated with a daily subcutaneous dose of HgCl2 (5.0mg/kg/day) or saline (0.9%). Twenty-four hours after the last HgCl2 administration, the animals were sacrificed and biological material was obtained. Concerning toxicity biomarkers, Hg exposure inhibited blood δ-aminolevulinic acid dehydratase (δ-ALA-D), serum alanine aminotransferase (ALT) activity and also increased serum creatinine levels. (PhSe)2 partially prevented blood δ-ALA-D inhibition and totally prevented the serum creatinine increase. Regarding the oxidative parameters, Hg decreased kidney TBARS levels and increased kidney non-protein thiol levels, while (PhSe)2 pre-treatment partially protected the kidney thiol levels increase. Animals exposed to HgCl2 presented Hg content accumulation in blood, kidney and liver. The (PhSe)2 pre-treatment increased Hg accumulation in kidney and decreased in blood. These results show that (PhSe)2 can be efficient in protecting against these toxic effects presented by this Hg exposure model.

Lactating and non-lactating rats differ in sensitivity to HgCl(2): Protective effect of ZnCl(2).

This work investigated zinc (Zn) and mercury (Hg) effects on oxidative parameters, markers of toxicity and metal levels in different tissues from non-lactating rats (NLR) and lactating rats (LR). Adult NLR and LR received ZnCl2 (27mg/kg) or saline (0.9%) subcutaneously and after 24h they received HgCl2 (5mg/kg) or saline (0.9%). Twenty four hours later, they were sacrificed and the preparation of biological material and biochemical analyses were performed. With respect to oxidative parameters, Hg exposure decreased kidney total SH levels from NLR and LR and hepatic catalase activity (not statistically significant) in NLR. Zinc pre-treatment partly prevented the decrease of kidney total SH levels in LR. Zinc per se increased hepatic non-protein SH levels of NLR and LR. Regarding toxicity markers, Hg exposure inhibited the δ-aminolevulinic acid dehydratase (δ-ALA-D) activity from kidney and liver of NLR, inhibited serum alanine aminotransferase (ALT) activity of LR and increased serum creatinine and urea levels of NLR and LR. Zinc pre-exposure prevented the enzymatic alterations caused by Hg. NLR and LR Hg exposed presented accumulation of mercury in the kidney, liver, blood and urine. Zinc pre-treatment prevented this accumulation partly in NLR liver and blood and completely in LR kidney and liver. These results show that NLR and LR are differently sensitive to HgCl2 and that ZnCl2 showed a promising effect against Hg toxicity.

Distinct response of lactating and nonlactating rats exposed to inorganic mercury on hepatic δ-aminolevulinic acid dehydratase activity.

This study investigated if lactating and nonlactating rats presented differences in relation to hepatic sensitivity to HgCl2 and the potential preventive role of ZnCl2. Lactating (days 3-12 of lactation) and nonlactating rats received 27 mg/kg ZnCl2 for five consecutive days and 5 mg/kg HgCl2 for five subsequent days. Lactating and nonlactating rats exposed to HgCl2 presented a decrease in food intake, a decrease in plasma alanine aminotransferase (ALT), and an increase in hepatic Hg levels when compared to the control group. Only lactating rats exposed to HgCl2 presented an increase in hepatic δ-aminolevulinic acid dehydratase activity. On the other hand, only nonlactating rats exposed to HgCl2 presented an increase in plasma aspartate aminotransferase (AST). ZnCl2 pre-exposure partially protected the increase in plasma AST activity presented by nonlactating rats and potentiated the liver Hg accumulation in lactating rats. Pups from the Sal-Hg and Zn-Hg groups showed a decrease in absolute liver weight and an increase in liver Hg levels. Summarizing, this study demonstrated that lactating rats presented distinct biochemical responses compared to nonlactating rats exposed to HgCl2 when hepatic parameters were evaluated.

Effects of chlorogenic acid, caffeine, and coffee on behavioral and biochemical parameters of diabetic rats.

Diabetes mellitus (DM) is associated with brain alterations that may contribute to cognitive dysfunctions. Chlorogenic acid (CGA) and caffeine (CA), abundant in coffee (CF), are natural compounds that have showed important actions in the brain. The present study aimed to evaluate the effect of CGA, CA, and CF on acetylcholinesterase (AChE), Na(+), K(+)-ATPase, aminolevulinate dehydratase (δ-ALA-D) activities and TBARS levels from cerebral cortex, as well as memory and anxiety in streptozotocin-induced diabetic rats. Animals were divided into eight groups (n = 5-10): control; control/CGA 5 mg/kg; control/CA 15 mg/kg; control/CF 0.5 g/kg; diabetic; diabetic/CGA 5 mg/kg; diabetic/CA 15 mg/kg; and diabetic/CF 0.5 g/kg. Our results demonstrated an increase in AChE activity and TBARS levels in cerebral cortex, while δ-ALA-D and Na(+), K(+)-ATPase activities were decreased in the diabetic rats when compared to control water group. Furthermore, a memory deficit and an increase in anxiety in diabetic rats were observed. The treatment with CGA and CA prevented the increase in AChE activity in diabetic rats when compared to the diabetic water group. CGA, CA, and CF intake partially prevented cerebral δ-ALA-D and Na(+), K(+)-ATPase activity decrease due to diabetes. Moreover, CGA prevented diabetes-induced TBARS production, improved memory, and decreased anxiety. In conclusion, among the compounds studied CGA proved to be a compound which acts better in the prevention of brain disorders promoted by DM.

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats.

The aim of the present study was to evaluate the possible effects of zinc chloride against the gastrointestinal lesions caused by oral administration of ethanol in rats. Rats were divided into five groups, namely, saline, ethanol, zn, zn+ethanol and ethanol+zn. Ethanol 70% (2 mL/kg) was administered by gavage in 36 h fasted rats. Zinc chloride (27 mg/kg, ~13 mg/kg of zinc) was given by gavage 1h before or 1h after the administration of ethanol. Oral administration of ethanol consistently induced damage in the rat glandular stomach and intestine. Zinc did not demonstrate effect per se and significantly reduced gastrointestinal lesions when administered either before or after lesion induction. Ethanol induced enhancement of thiobarbituric acid reactive substance and reactive species levels, diminished the ascorbic acid and total protein SH content as well as superoxide dismutase and catalase activity in stomach and intestine of rats. Zinc treatment prevented and reversed these alterations induced by ethanol. Stomach and intestine of rats treated with zinc presented higher zinc content than the tissues of rats treated only with ethanol. Non-protein SH content was not altered by any treatment. Results suggested that the gastrointestinal protective effect of zinc in this experimental model could be due to its antioxidant effect.

Effectiveness of copper chloride in protecting against alterations induced by mercury chloride in newborn rats.

This work investigated the effects of copper as preventive treatment against mercury-induced alterations in young rats. Wistar rats were treated (subcutaneous) with saline or CuCl(2) · 2H(2) O (6.9 mg/kg/day) from 3 to 7 days old and with saline or HgCl(2) (5.0 mg/kg/day) from 8 to 12 days old. Rats were sacrificed 24 h after the last dose. Mercury-exposed rats presented inhibition of liver (43%) and kidney (52%) porphobilinogen (PBG)-synthase activity and serum lactic dehydrogenase activity (50%). Also, an increase of the serum creatinine and urea levels around threefold and fivefold was observed, respectively. Pre-exposure to copper partially prevented the mercury effect on liver but not on kidney PBG synthase, and prevented the increase of the creatinine levels. Blood and brain PBG synthase and serum alanineaminotransferase activities, as well as glycemia, and liver glycogen content were not altered by treatments. These results show that copper, although being an essential metal, is inefficient as a preventive agent against mercury poisoning in parameters investigated after the end of mercury exposure.