RESUMO
Aquaculture activities in southern Chile demand floating devices to produce electricity powered by diesel generators. It has been recently proposed to replace this fuel with propane. However, little is known about the behaviour and possible environmental impacts of an accidental release of propane underwater. In this study we evaluated the impact of water temperature and salinity on the saturation and further release of propane under controlled laboratory experiments. Results showed that under extreme environmentally relevant scenarios (high and low temperature and salinity), propane saturated the water more quickly. However, while it is important to consider that saturation times can be similar (â¼2 h), the magnitudes of propane dissolved can be different. Experiments showed that cold waters (5 °C) propane is dissolved twice than warm waters (20 °C). Residence time was more affected by water temperature and almost independent of water salinity. Propane may take at least 2 days to be released from waters (around 90% of the initial amount dissolved under laboratory conditions). Additionally, we evaluated the impact on dissolved oxygen displacement and the embryotoxicity of the dissolved fraction by using Zebrafish Embryo Toxicity Assay. Results showed that dissolved oxygen was quickly removed. However, the levels of dissolved oxygen were promptly recovered in the studied systems. We also observed that propane can generate genotoxic effects (3-10% mortality), but after 2 days the system can be almost free of propane and the effects may become much lower. Comparatively with the literature, propane showed to be less toxic than diesel and it is a viable and less environmentally hazardous replacement for diesel.
Assuntos
Propano , Peixe-Zebra , Animais , Chile , Meio Ambiente , Propano/toxicidade , SalinidadeRESUMO
The in vitro effect of (E)-2-benzylidene-4-phenyl-1,3-diselenole (BPD) was evaluated through iron/EDTA-induced thiobarbituric acid reactive species (TBARS) and reactive species (RS) determinations as well as of the scavenging 2,2'-diphenyl-1-picrylhydrazyl (DPPH) radical quantification. BPD at the concentrations of 10 and 50 µΜ decreased RS and TBARS levels, respectively. The antioxidant activity was not related to the scavenging DPPH radical mechanism. A second objective of this study was to investigate the hepatoprotective action of BPD, administered by oral route, against oxidative damage induced by 2-nitropropane (2-NP) (100 mg/kg of body weight) in liver of rats. At the dose of 50 mg/kg, BPD protected against the increase in aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) activities induced by 2-NP. BPD (10 and 50 mg/kg) protected against the increase in TBARS levels and alkaline phosphatase (ALP) activity. Sections of liver from 2-NP-exposed rats presented intense infiltration of inflammatory cells and loss of cellular architecture. BPD (10 and 50 mg/kg) attenuated 2-NP-induced hepatic histological alterations. The inhibition of δ-aminolevulinic dehydratase (δ-ALA-D), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione S-transferase (GST) activities and the decreased GSH levels caused by 2-NP were protected by BPD (50 mg/kg). Catalase activity and ascorbic acid levels were not altered by 2-NP. These results demonstrated the antioxidant and hepatoprotective effects of BPD in liver of rats.
Assuntos
Antioxidantes/farmacologia , Fígado/efeitos dos fármacos , Compostos Organosselênicos/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Administração Oral , Animais , Antioxidantes/administração & dosagem , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Sequestradores de Radicais Livres/administração & dosagem , Sequestradores de Radicais Livres/farmacologia , Fígado/patologia , Masculino , Nitroparafinas/toxicidade , Compostos Organosselênicos/administração & dosagem , Propano/análogos & derivados , Propano/toxicidade , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
Organoselenides have been documented as promising pharmacological agents against a number of diseases associated with oxidative stress. Here we have investigated, for the first time, the potential antioxidant activity of binaphthyl diselenide ((NapSe)(2); 50 mg kg(-1), p.o.) against the 2-nitropropane (2-NP)-induced hepatoxicity in rats, using different end points of toxicity (liver histopathology, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine). In addition, in view of the association of oxidative stress with 2-NP exposure, hepatic lipid peroxidation, ascorbic acid levels, delta-aminolevulinate dehydratase (delta-ALA-D) and catalase (CAT) activities were evaluated. 2-NP caused an increase of AST, ALT and hepatic lipid peroxidation. 2-NP also caused hepatic histopathological alterations and delta-ALA-D inhibition. (NapSe)(2) (50 mg kg(-1)) prevented 2-NP-induced changes in plasmatic ALT and AST activities and also prevented changes in hepatic histology, delta-ALA-D and lipid peroxidation. Results presented here indicate that the protective mechanism of (NapSe)(2) against 2-NP hepatotoxicity is possibly linked to its antioxidant activity.
Assuntos
Antioxidantes/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Compostos Organosselênicos/farmacologia , Alanina Transaminase/metabolismo , Animais , Antioxidantes/química , Ácido Ascórbico/metabolismo , Aspartato Aminotransferases/metabolismo , Catalase/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Creatinina/metabolismo , Peroxidação de Lipídeos , Nitroparafinas/toxicidade , Compostos Organosselênicos/química , Estresse Oxidativo , Sintase do Porfobilinogênio/metabolismo , Propano/análogos & derivados , Propano/toxicidade , RatosRESUMO
The aim of this study was to investigate the protective effect of 3-alkynyl selenophene (3-ASP) on acute liver injury induced by carbon tetrachloride (CCl(4)) and 2-nitropropane (2-NP) in rats. On the first day of treatment, the animals received 3-ASP (25 mg/kg, p.o.). On the second day, the rats received CCl(4) (1 mg/kg, i.p.) or 2-NP (100 mg/kg, p.o.). Twenty-four hours after CCl(4) or 2-NP administration, the animals were euthanized, and their plasma and liver were removed for biochemical and histological analyses. The histological analysis revealed extensive injury in the liver of CCl(4)-exposed and 2-NP-exposed rats, which was attenuated by 3-ASP. 3-ASP significantly attenuated (1) the increase in plasmatic aspartate and alanine aminotransferase activities and lipid peroxidation levels induced by CCl(4) and 2-NP; (2) the inhibition of δ-aminolevulinic dehydratase activity caused by 2-NP; and (3) the decrease in ascorbic acid (AA) levels and catalase (CAT) activity caused by CCl(4). AA levels and CAT activity remained unaltered in the liver of rats exposed to 2-NP. The protective effect of 3-ASP on acute liver injury induced by CCl(4) and 2-NP in rats was demonstrated.
Assuntos
Alcinos/uso terapêutico , Tetracloreto de Carbono/toxicidade , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Nitroparafinas/toxicidade , Compostos Organosselênicos/uso terapêutico , Propano/análogos & derivados , Substâncias Protetoras/uso terapêutico , Alcinos/farmacologia , Animais , Ácido Ascórbico/metabolismo , Catalase/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/anatomia & histologia , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Compostos Organosselênicos/farmacologia , Propano/toxicidade , Substâncias Protetoras/farmacologia , Ratos , Ratos WistarRESUMO
This study was undertaken to investigate if the introduction of trifluoromethyl (F(3)C) group into diphenyl diselenide (PhSe)(2) molecule causes acute toxicity in rats. It was further examined if the presence of F(3)C group in (PhSe)(2) molecule alters the protective effect caused by (PhSe)(2) against damage induced by 2-nitropropane (2-NP) in rats. To investigate the potential oral toxicity of (PhSe)(2) and (F(3)CPhSe)(2), rats received a single oral application of (PhSe)(2) (7.8-312 mg/kg) or (F(3)CPhSe)(2) (11.2-448 mg/kg). Calculated lethal dose (LD(50)) for (PhSe)(2) and (F(3)CPhSe)(2) was estimated to be 312 mg/kg (=1 mmol/kg) and 234 mg/kg (=0.52 mmol/kg), respectively. Oral administration of (PhSe)(2) in rats did not change plasma alanine and aspartate aminotransferase activities (AST and ALT) as well as urea and creatinine levels. The introduction of F(3)C group into (PhSe)(2) molecule increased AST activity in plasma of rats. (PhSe)(2) (3.2 mg/kg=10 micromol/kg) and (F(3)CPhSe)(2) (4.48 mg/kg=10 micromol/kg) protected ALT, AST and gamma-glutamyl transferase (gamma-GT) activities against the increase caused by oral administration of 2-NP (120 mg/kg) in rats. (PhSe)(2) and (F(3)CPhSe)(2) ameliorated hepatic catalase activity altered by 2-NP in rats. These results indicate that the chemical alteration into (PhSe)(2) molecule introduced toxicity and altered its protective effect against damage induced by 2-NP in rats.
Assuntos
Derivados de Benzeno/química , Derivados de Benzeno/toxicidade , Rim/efeitos dos fármacos , Fígado/efeitos dos fármacos , Nitroparafinas/toxicidade , Compostos Organosselênicos/química , Compostos Organosselênicos/toxicidade , Propano/análogos & derivados , Alanina Transaminase/efeitos dos fármacos , Animais , Aspartato Aminotransferases/efeitos dos fármacos , Dose Letal Mediana , Masculino , Propano/toxicidade , Ratos , Ratos Wistar , gama-Glutamiltransferase/efeitos dos fármacosRESUMO
The nematocide 1,2-dibromo-3-chloropropane (DBCP), widely used in Costa Rica during the late 1960s and 1970s, causes sterility in men and is a possible carcinogen. Mortality among a cohort of Costa Rican banana plantation workers was investigated. The cohort included 40,959 individuals who worked on banana plantations between 1972 and 1979. Employment records were linked with the Costa Rican Mortality Registry to determine outcomes through 1999. Standardized mortality ratios (SMRs) were calculated for all causes of death. Poisson regression was also used to calculate mortality risk estimates by duration of employment, but provided no additional insight. All-causes SMRs were 0.77 for men (95% CI 0.75-0.80) and 0.90 for women (95% CI 0.80-1.02) relative to national mortality rates. Mortality from septicemia was significantly higher than expected. Nonsignificant increases in mortality were also observed for testicular cancer, penile cancer, Hodgkin's disease, and Parkinson's disease in men, and for cervical cancer and lung cancer in women.
Assuntos
Doenças dos Trabalhadores Agrícolas/mortalidade , Propano/análogos & derivados , Estudos de Coortes , Costa Rica/epidemiologia , Feminino , Humanos , Masculino , Musa , Distribuição de Poisson , Propano/toxicidade , Estudos RetrospectivosRESUMO
The effect of post-treatment with diphenyl diselenide on liver damage induced by 2-nitropropane (2-NP) was examined in male rats. Rats were pre-treated with a single dose of 2-NP (100 mg/kg body weight dissolved in canola oil). Afterward, the animals were post-treated with a dose of diphenyl diselenide (10, 50 or 100 micromol/kg). The parameters that indicate tissue damage such as liver histopathology, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), urea and creatinine were determined. Since the liver damage induced by 2-NP is related to oxidative damage, lipid peroxidation, superoxide dismutase (SOD), catalase (CAT) and ascorbic acid level were also evaluated. Diphenyl diselenide (50 and 100 micromol/kg) effectively restored the increase of ALT and AST activities and urea level when compared to the 2-NP group. At the higher dose, diphenyl diselenide decreased GGT activity. Treatment with diphenyl diselenide, at all doses, effectively ameliorated the increase of hepatic and renal lipid peroxidation when compared to 2-NP group. 2-NP reduced CAT activity and neither alter SOD activity nor ascorbic acid level. This study points out the involvement of CAT activity in 2-NP-induced acute liver damage and suggests that the post-treatment with diphenyl diselenide was effective in restoring the hepatic damage induced by 2-NP.
Assuntos
Antioxidantes/farmacologia , Derivados de Benzeno/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Fígado/efeitos dos fármacos , Nitroparafinas/toxicidade , Compostos Organosselênicos/farmacologia , Propano/análogos & derivados , Solventes/toxicidade , Doença Aguda , Animais , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Interações Medicamentosas , Enzimas/metabolismo , Sequestradores de Radicais Livres , Rim/efeitos dos fármacos , Rim/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Testes de Função Hepática , Masculino , Propano/toxicidade , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismoRESUMO
The effect of diphenyl diselenide, (PhSe)2, administration on 2-nitropropane (2-NP)-induced hepatic damage was examined in male rats. Rats were pre-treated with a single dose of diphenyl diselenide (10, 50 or 100 micromol/kg). Afterward, they received only one dose of 2-NP (100 mg/kg body weight dissolved in olive oil). The parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alpha-fetoprotein (AFP), creatinine and urea were determined. Since toxicity induced by 2-NP is related to oxidative stress, lipid peroxidation was also evaluated. Diphenyl diselenide (100 micromol/kg) significantly reduced plasma ALT, gamma-GGT, AFP levels when compared to 2-NP group. Treatment with diphenyl diselenide, at all doses, effectively protects the increase of lipid peroxidation when compared to 2-NP group. Histological examination revealed that 2-NP treatment causes a moderate swelling and degenerative alterations on hepatocytes and diphenyl diselenide (100 micromol/kg) protects against these alterations. Diphenyl diselenide (50 and 100 micromol/kg) significantly decreased the urea level. This study evidences the protective effect of diphenyl diselenide by 2-NP-induced acute hepatic damage.