Environmental cadmium exposure and metabolic responses of the Nile tilapia, Oreochromis niloticus

The contamination of water by metal compounds is a worldwide environmental problem. This study was undertaken to evaluate the impact of short-term cadmium exposure on metabolic patterns of the freshwater fish Oreochromis niloticus. The fish were exposed to 320, 640, 1280 and 2560 mug/l sublethal concentrations of Cd++ (CdCl2) in water for 7 days. The specific activities of the enzymes phosphofructo kinase (PFK-E.C.2.7.1.11.), lactate dehydrogenase (LDH-E.C.1.1.1.27.) and creatine kinase (CK-E.C.2.7.3.2.) were decreased in white muscle after cadmium treatments, indicating decreases in the capacity of glycolysis in this tissue. Cadmium exposure induced increased glucose concentration in white muscle of fish. on the other hand, cadmium exposure at sublethal concentrations increased phosphofructo kinase and LDH in red muscle of fish. Cadmium significantly decreased total protein concentrations in liver and white muscle regardless of tissue glycogen levels. The data suggest that cadmium acts as a stressor, leading to metabolic alterations similar to those observed in starvation. (C) 2001 Elsevier B.V. Ltd. All rights reserved.

VIABILITY of SPORULATED OOCYSTS of NEOSPORA CANINUM AFTER EXPOSURE TO DIFFERENT PHYSICAL and CHEMICAL TREATMENTS

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cadmium and exposure to stress increase aggressive behavior

Environmental toxicants and stress influence the health and behavior of people from different parts of the world. In the present study, aggressive behavior was evaluated in rats exposed to cadmium (Cd) for four weeks and subjected to immobilization stress (IS) based on the resident/intruder paradigm. Latency to the first bite (LB), total number of attacks (NA), total duration of attack manifestations (DAM), and a composite aggression score (CAS) were used to assess aggressiveness. Cadmium concentrations in the blood and the brain were determined. We observed that the parameters of aggressiveness were not altered by either Cd or IS when administered separately. However, animals exposed to Cd + IS had increased NA, DAM, and CAS. Cadmium was detected in the blood and the brain after treatment and Cd + IS exposure modified Cd distribution in these tissues. These results suggest that exposure to low levels of Cd associated with stress may lead to increased aggressiveness in rats. (C) 2011 Elsevier B.V. All rights reserved.

Evaluation of developmental changes in bovine in vitro produced embryos following exposure to bovine Herpesvirus type 5

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of acute cold exposure on rectal temperature, blood glucose and plasma free fatty acids in alloxan-diabetic rats

These experiments were carried out to study the effects of acute cold exposure (0-2°C/4 hr) on rectal temperature, blood glucose and plasma free fatty acids (FFA) in alloxan-diabetic rats. Male Wistar rats weighing 170-190 g were used and diabetes was induced by i.v. alloxan injection (40 mg/kg body wt). Cold exposure produced severe hypothermia in diabetic rats. After 4 hr of cold, blood glucose of diabetic rats was reduced from 296±16 to 86t±12 mg/dl (P<0.01), and FFA increased slightly, but was not statistically different (P>0.05) from the initial value. As expected, interscapular brown adipose tissue (IBAT) and retroperitoneal and epididymal white adipose tissues were significantly lower in diabetic than in control rats. Cold exposure reduced total IBAT lipids in control but not in diabetic animals. The results of this experiment suggest that diabetic rats were unable to maintain body temperature in the cold, probably because of a failure to generate an adequate amount of heat by nonshivering thermogenesis in brown adipose tissue.

Toxic effects of nickel exposure on heart and liver of rats

The role of air pollution as a health risk factor is of special interest. Numerous toxic pollutants, such as nickel, are being released to the environment as a result of combustion of fossil fuels, crude oil, and coal. Nickel in the atmosphere can be combined with other environmental pollutants, producing various nickel compounds, which have varying animal toxicity. A rat biossay validated for the identification of toxic effects of nickel revealed increased serum activities of total lactate dehydrogenase (LDH) and alanine transaminase (ALT) in rats that received intratracheal injection of Ni2+ in .09% saline solution of NiCl2. The total LDH activity was also increased in the heart, and the isoenzyme pattern showed the LDH1/LDH2 ratio elevated to greater than 1. We conclude that intratracheal administration of nickel induced cardiac and hepatic damage. The development of cardiac and hepatic damage and of increased enzymes' activities was only demonstrated when nickel had accumulated in these tissues, indicating that nickel depot is essential to its toxicity. Intratracheal administration of NiCl2 induced changes in LDH and ALT activities.

Developmental and behavioral effects of postnatal amitraz exposure in rats

The effects of postnatal amitraz exposure on physical and behavioral parameters were studied in Wistar rats, whose lactating dams received the pesticide (10 mg/Kg) orally on days 1, 4, 7, 10, 13, 16 and 19 of lactation; control dams received distilled water (1 ml/kg) on the same days. A total of 18 different litters (9 of them control and 9 experimental) born after a 21- day gestation were used. The results showed that the median effective time (ET50) for fur development, eye opening, testis descent and onset of the startle response were increased in rats postnatally exposed to amitraz (2.7, 15.1, 21.6 and 15.3 days, respectively) compared to those of the control pups (1.8, 14.0, 19.9 and 12.9 days, respectively). The ages of incisor eruption, total unfolding of the external ears, vaginal and ear opening and the time taken to perform the grasping hindlimb reflex were not affected by amitraz exposure. Pups from dams treated with amitraz during lactation took more time (in seconds) to perform the surface righting reflex on postnatal days (PND) 3 (25.0 ±2.0), 4 (12.3 ± 1.2) and 5 (8.7 ± 0.9) in relation to controls (10.6 ± 1.2; 4.5 ± 0.6 and 3.4 ± 0.4, respectively); the climbing response was not changed by amitraz. Postnatal amitraz exposure increased spontaneous motor activity of male and female pups in the open-field on PND 16 (140± 11)and 17(124± 12), and 16 (104±9), 17 (137 ± 9) and 18 (106 ± 8), respectively. Data on spontaneous motor activity of the control male and female pups were 59 ± 11 and 69 ± 10 for days 16 and 17 and 49 ± 9, 48 ± 7 and 56 ± 7 for days 16, 17 and 18, respectively. Some qualitative differences were also observed in spontaneous motor behavior; thus, raising the head, shoulder and pelvis matured one or two days later in the amitraz- treated offspring. Postnatal amitraz exposure did not change locomotion and rearing frequencies or immobility time in the open-field on PND 30, 60 and 90. The present findings indicate that postnatal exposure to amitraz caused transient developmental and behavioral changes in the exposed offspring and suggest that further investigation of the potential health risk of amitraz exposure to developing human and animal offsprings may be warranted.

Superoxide radical and nephrotoxic effect of cadmium exposure

Pollution and industrial practices result in concentrations of metals and other environmental agents that are related to environmental toxicity. Concentrations of metals are widely related to biochemicals values which are used in disease diagnosis due to environmental toxicity. This work was carried out in order to verify the nephrotoxic effect of cadmium and to clarify the contribution of reactive oxygen species (ROS) in this process. Cadmium chloride was tested for nephrotoxic damage in rats by a single intraperitoneal (i.p.) injection Cd 2+ (2 mg/kg) and oral intake (Cd2 +-100 mg/l-from CdCl 2). The cadmium-induced biochemical alterations included significant increased levels of serum creatinine concentrations, in rats with i.p. injection. Total urinary protein concentrations were only increased in rats with cadmium intake. Lipoperoxide was also increased after 3 and 7 days of the Cd 2+ treatment. No changes were observed in glutathione peroxidase activities. Cadmium-induced damage might be due to superoxide radicals (O 2 -), since Cu-Zn superoxide dismutase activities were decreased by Cd 2+ treatment. This study allows tentative conclusions to be drawn regarding which reactive oxygen metabolites play a role in cadmium nephrotoxicity. We concluded that the superoxide radical may be produced as a mediator of nephrotoxic action of cadmium.

Effect of α-tocopherol on superoxide radical and toxicity of cadmium exposure

Contamination with cadmium compounds poses high potential risk for the health of populations and for this reason the treatment of their toxic effects should urgently be established. The present study was carried out to determine whether α-tocopherol intake can protect tissues against damage induced by cadmium, and to clarify the contribution of superoxide radicals (O 2 -) in this process. Cadmium chloride was tested for tissue damage by a single intraperitoneal injection of Cd 2+ ions (2 mg Kg -1). To determine the potential therapeutic effect of vitamin E, a group of Cd 2+-treated rats received a drinking solution of α-tocopherol (40 mg l -1) for 15 days. Cadmium induced increased serum creatinine and total lactate dehydrogenase, reflecting renal and cardiac damage. The increased lipoperoxide and decreased Cu-Zn superoxide dismutase levels indicated the generation of superoxide radicals in cadmium-treated rats. Tocopherol induced increased serum high-density lipoprotein and depressed the toxic effects of Ca 2+ alone, since creatinine and lactate dehydrogenase determinations were recovered to the control values. Tocopherol decreased lipoperoxide and led the superoxide dismutase activities to approach those of the control values. We concluded that superoxide radicals are produced as mediators of cadmium toxicity. Tocopherol possesses a significant anti-radical activity and inhibits the cadmium effect on superoxide dismutase activity. Tocopherol also protected tissues from the toxic effects of cadmium by a direct antioxidant action which decreased lipoperoxide formation.

Toxic mechanism of nickel exposure on cardiac tissue

The incidence of cardiovascular disease has increased in the general population, and cardiac damage is indicated as one important cause of mortality. In addition, pollution and metal exposure have increased in recent years. For this reason, toxic effects of metals, such as nickel, and their relation to cardiac damage should be urgently established. Although free radical-mediated cellular damage and reactive oxygen species have been theorized as contributing to the nickel mechanism of toxicity, recent investigations have established that free radicals may be important contributors to cardiac dysfunction. However, there is little information on the effect of nickel exposure on markers of oxidative stress in cardiac tissue. Nickel exposure (Ni2+ 100 mg L-1 from NiSO4) significantly increased lipoperoxide and total lipid concentrations in cardiac tissue. We also observed increased serum levels of cholesterol (59%), lactate dehydrogenase (LDH-64%), and alanine transaminase (ALT-30%) in study animals. The biochemical parameters recovered to the control values with tocopherol intake (0.2 mg 200 g-1). Vitamin E alone significantly decreased the lipoperoxide concentration and increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the heart. Since no alterations were observed in catalase and GSH-Px activities by nickel exposure while SOD activities were decreased, we conclude that superoxide radical (O2 -) generated by nickel exposure is of primary importance in the pathogenesis of cardiac damage. Tocopherol, by its antioxidant activity, decreased the toxic effects of nickel exposure on heart of rats.

Toxic mechanism of cadmium exposure on cardiac tissue

The presence of toxic substances in the workplace environment requires systematic evaluation of exposure and health status in exposed subjects. Cadmium is a highly toxic element found in water. Although free mediated cellular damage and reactive oxygen species (ROS), had been theorized as contributing to the cadmium mechanism of toxicity, and recent investigations have established that free radicals may be important contributors to cardiac dysfunction, there is little information on the effect of cadmium exposure on markers of oxidative stress in cardiac tissue. Cadmium exposure (Cd2+ - 100 mg/1-from CdCl2) in drinking water, during 15 days, significantly increased lipoperoxide and decreased the activities of superoxide dismutase and glutathione peroxidase. No alterations were observed in catalase activity in heart of rats with cadmium exposure. We also observed decreased glycogen and glucose concentration and increased total lipid content in cardiac tissue of rats with cadmium exposure. The decreased activities of alanine transaminase and aspartate transaminase reflected decreased metabolic protein degradation, and increased lactate dehydrogenase activity was related with increases in capacity of glycolysis. Since the metabolic pathways were altered by cadmium exposure, we can conclude that Cd2+ exposure induced ROS and initiate some series of events that occur in the heart and resulted in metabolic pathways alterations.

Occupational exposure to paint solvents and particulate material in car repair shops

Aims: We evaluated solvents and total particulates exposures in auto body repair shops together with a search of painter's related complaints. Methods: 26 painters exposures were evaluated by pumped personal sampling; solvents were retained in charcoal sorbent tubes and the particulates in PVC filters. Painter's personal habits and their work characteristics were obtained through a questionnaire, applied in a private interview. For the symptoms the Q16 questionnaire was used, added of questions about complaints during the painting. Results: High exposures were detected during spray painting. For solvents, the TLV-STEL adjusted for the mixtures was surpassed in six evaluations. However, as repaint is a short-term operation, it makes the average concentrations weighed for the work shift lower than the TLV-TWA adjusted for the mixtures. Total particulate concentrations had surpassed the TLV-TWA in four of the evaluations. Symptoms frequency in the Q16 questionnaire was higher for painters than for the controls (Mann-Whitney test U=193; p=0.008), and they showed positive correlations with the age (Spearman r=0.354, t=1.85, p=0.076), the number of years in the profession (Spearman r=0.433, t=2.35, p=0.027) and the alcoholic beverage consumption (Spearman r=0.457, t=2.516, p=0.019). Conclusions: The painting work done at car repair shops can result in high solvent and particulate exposures, although they are short-term operations. Their acute and chronic effects for the painters do not have been clearly evidenced in the present study, continuing deserving multidisciplinary attention.

Tensile bond strength of self-etching versus total-etching adhesive systems under different dentinal substrate conditions

The use of acid etchants to produce surface demineralization and collagen network exposure, allowing adhesive monomers interdiffusion and consequently the formation of a hybrid layer, has been considered the most efficient mechanism of dentin bonding. The aim of this study was to compare the tensile bond strength to dentin of three adhesive systems, two self-etching ones (Clearfil SE Bond - CSEB and One Up Bond F - OUBF) and one total-etching one (Single Bond - SB), under three dentinal substrate conditions (wet, dry and re-wet). Ninety human, freshly extracted third molars were sectioned at the occlusal surface to remove enamel and to form a flat dentin wall. The specimens were restored with composite resin (Filtek Z250) and submitted to tensile bond strength testing (TBS) in an MTS 810. The data were submitted to two-way ANOVA and Tukey's test (p = 0.05). Wet dentin presented the highest TBS values for SB and CSEB. Dry dentin and re-wet produced significantly lower TBS values when using SB. OUBF was not affected by the different conditions of the dentin substrate, producing similar TBS values regardless of the surface pretreatments.

Historical and recent biological markers of exposure to fluoride

Recent and historical biomarkers assess chronic or subchronic exposure to fluoride. The most studied recent biomarkers are nails and hair. Both can be non-invasively obtained, although collection of nails is more accepted by the subjects. External contamination may be a problem for both biomarkers and still needs to be better evaluated. Nails have been more extensively studied. Although the available knowledge does not allow their use as predictors of dental fluorosis by individual subjects, since reference values of fluoride have not yet been established, they have a strong potential for use in epidemiological surveys. Toenails should be preferred instead of fingernails, and variables that are known to affect nail fluoride concentrations - such as age, gender and geographical area - should be considered. The main historical biomarkers that could indicate total fluoride body burden are bone and dentin. Of these, bone is more studied, but its fluoride concentrations vary according to the type of bone and subjects' age and gender. They are also influenced by genetic background, renal function and remodeling rate, variables that complicate the establishment of a normal range of fluoride levels in bone that could indicate 'desirable' exposure to fluoride. The main issue when attempting to use bone as biomarker of fluoride exposure is the difficulty and invasiveness of sample collection. In this aspect, collection of dentin, especially from 3rd molars that are commonly extracted, is advantageous. However, mean values also span a wide range and reference concentrations have not been published yet. © 2011 S. Karger AG, Basel.

Ethopharmacological evaluation of the rat exposure test: A prey-predator interaction test

The rat exposure test (RET) is a prey (mouse)-predator (rat) situation that activates brain defensive areas and elicits hormonal and defensive behavior in the mouse. Here, we investigated possible correlations between the spatiotemporal [time spent in protected (home chamber and tunnel) and unprotected (surface) compartments and frequency of entries into the three compartments] and ethological [e.g., duration of protected and unprotected stretched-attend postures (SAP), duration of contact with the rat's compartment] measures (Experiment 1). Secondly, we investigated the effects of systemic treatment with pro- or anti-aversive drugs on the behavior that emerged from the factor analysis (Experiment 2). The effects of chronic (21 days) imipramine and fluoxetine on defensive behavior were also investigated (Experiment 3). Exp. 1 revealed that the time in the protected compartment, protected SAP and rat contacts loaded on factor 1 (defensive behavior), while the total entries and unprotected SAP loaded on factor 2 (locomotor activity). Exp. 2 showed that alprazolam (but not diazepam) selectively changed the defensive factor. Caffeine produced a mild proaversive-like effect, whereas yohimbine only decreased locomotor activity (total entries). Fluoxetine (but not imipramine) produced a weak proaversive-like effect. 5-HT1A/5-HT2 receptor ligands did not change any behavioral measure. In Exp. 3, chronic fluoxetine (but not imipramine) attenuated the defensive behavior factor without changing locomotion. Given that the defensive factor was sensitive to drugs known to attenuate (alprazolam and chronic fluoxetine) and induce (caffeine) panic attack, we suggest the RET as a useful test to assess the effects of panicolytic and panicogenic drugs. © 2012 Elsevier B.V.