I.S. Rabitto

Mercury and DDT exposure risk to fish-eating human populations in Amazon

In order to investigate the potential risk of mercury and DDTs exposure to fish-eating human populations in Samuel Reservoir, not affected directly by gold-mining activities, the axial muscle of Cichla monoculus was analyzed. Twenty-nine and thirty adults individuals were collected respectively on February (rainy season) and August (dry season) 2007. The specimens were sacrificed by spinal section before sex identification, body weight and total length determination. For total mercury, DDT and DDE quantifications and cholinesterase activity samples of the axial muscle were frozen at -20°C, and for histopathological studies gill and liver were fixed in ALFAC solution for 16 h. A value of 48.2% and 33% of the individuals, respectively from rainy and dry seasons, presented mercury concentrations higher than the maximum established for safe human consumption (0.5 μg g⁻¹) by World Health Organization. A positive correlation between body weight and Hg concentration was observed only in individuals from the rainy season, but no correlation was observed to DDT and DDE from both seasons. Differently from that observed to mercury, DDT levels presented a significant difference between both studied seasons, but no correlation was observed for both mercury and DDTs and sex. The levels of DDTs in muscle of C. monoculus are under the maximum established by FAO-Alimentarius CODEX and Swedish Food Regulation for human consumption. The histopathological and neurotoxic findings showed that the wild population of fish is affected by chronic exposure to mercury, meaning risk also to fish-eating populations. Finally, the results showed that C. monoculus is an important vehicle for human exposure to mercury and DDTs in Samuel Reservoir and that it is necessary a continuous biomonitoring of the levels of both pollutants in order to manage the risk of exposure to human populations.

The FXR agonist 6ECDCA reduces hepatic steatosis and oxidative stress induced by ethanol and low-protein diet in mice

BACKGROUND AND AIM Excessive ethanol consumption can lead to development of hepatic steatosis. Since the FXR receptor regulates adipose cell function and liver lipid metabolism, the aim of this work was to examine the effects of the FXR agonist 6ECDCA on alcoholic liver steatosis development and on oxidative stress induced by ethanol consumption. METHODS Swiss mice (n=24) received a low-protein diet (6%) and a liquid diet containing 10% ethanol or water for 6weeks. In the last 15days mice received oral treatment with 6ECDCA (3mgkg(-1)) or 1% tween (vehicle). The experimental groups (n=6) were: water+tween, water+6ECDCA, ethanol+tween and ethanol+6ECDCA. Moreover, as a diet control, we used a basal group (n=6), fed by a normal-proteic diet (23%) and water. After the treatment period, the animals were anesthetized for sample collection to perform plasma biochemistry assays, hepatic oxidative stress assays, hepatic cholesterol and triglycerides measurements, liver histology and hepatic gene expression. RESULTS Ethanol associated with low-protein diet induced hepatic oxidative stress, increased plasma transaminases and induced hepatic lipid accumulation. Many of these parameters were reversed by the administration of 6ECDCA, including amelioration of lipid accumulation and lipoperoxidation, and reduction of reactive oxygen species. These effects were possibly mediated by regulation of Srebpf1 and FAS gene expression, both reduced by the FXR agonist. CONCLUSIONS Our data demonstrated that 6ECDCA reverses the accumulation of lipids in the liver and decreases the oxidative stress induced by ethanol and low-protein diet. This FXR agonist is promising as a potential therapy for alcoholic liver steatosis.

Risks of waterborne copper exposure to a cultivated freshwater Neotropical catfish (Rhamdia quelen)

As it is the case in all animal food production systems, it is often necessary to treat farmed fish for diseases and parasites. Quite frequently, fish farmers still rely on the aggressive use of copper to control bacterial infections and infestations by ecto-parasites, and to manage the spread of diseases. The susceptibility of the neotropical fish Rhamdia quelen to copper was here evaluated at different waterborne copper concentrations (2, 7 or 11 μg Cu L(-1)) for 96 h, through a multi biomarkers approach. Liver histopathological findings revealed leukocyte infiltration, hepatocyte vacuolization and areas of necrosis, causing raised levels of lesions upon exposure to 7 and 11 μg Cu L(-1). Decreased occurrence of free melano-macrophages and increased densities of melano-macrophage centers were noted upon exposure to 11 μg Cu L(-1). Gills showed damages on their secondary lamellae already at 2 μg Cu L(-1); hypertrophy and loss of the microridges of pavement cells at 7 and 11 μg L(-1), and increased in chloride cell (CC) apical surface area (4.9-fold) and in CC density (1.5-fold) at 11 μg Cu L(-1). In the liver, catalase (CAT), glutathione peroxidase activities (GPx) and glutathione concentration (GSH) remained unchanged, compared to the control group. However, there was inhibition of 7-ethoxyresorufin-O-deethylase (EROD) at all copper concentrations tested. Glutathione reductase activity (GR) was reduced and levels of lipid peroxidation (LPO) were increased at 11 μg Cu L(-1). Glutathione S-transferase activity (GST) at 7 μg Cu L(-1) and superoxide dismutase activity (SOD) at both 7 and 11 μg Cu L(-1) were reduced. However, copper exposure did not alter brain and muscle acetylcholinesterase (AChE) activity. Osmoregulatory function was also disturbed, in agreement with the above-mentioned changes noted in the gills, as detected by plasma osmolality reduction in the group exposed to 11 μg Cu L(-1), and plasma chloride reduction at 2 μg Cu L(-1). These concentrations also, coherently, lead to inhibition of branchial carbonic anhydrase activity. In the kidney, increased carbonic anhydrase activity was measured in the groups exposed to 2 and 7 μg Cu L(-1). When these effects are compared to data available in the literature for other freshwater fish, also for 96 h of exposure, R. quelen appears as a relatively sensitive species. In addition, the concentrations employed here were quite low in comparison to levels used for disease control in real culture practices (ranging from 4 μg Cu L(-1) used against bacteria to 6000 μg Cu L(-1) against fungal infections). We can conclude that the concentrations frequently employed in aquaculture are in fact not safe enough for this species. Such data are essential for the questioning and establishment of new policies to the sector.

Alcoholic liver steatosis in mice is aggravated by low-protein diet and reversed by FXR agonist

Background Hepatic steatosis refers to the accumulation of triglycerides in hepatocytes, and it can be attributed to excessive ethanol consumption. The liver is the main organ of ethanol biotransformation and therefore, it can suffer with oxidative stress generated by ethanol. Since the FXR agonist 6ECDCA regulates adipose cell function, the aim of this work is to evaluate the participation of oxidative stress in ethanol-induced liver lesions and test the effects of FXR agonist against alcoholic liver steatosis development. For thus, diets with different amount of protein were used.