RESUMO

Modern nano-engineered pesticides have great promise for agriculture due to their extended, low dose release profiles that are intended to increase effectiveness but reduce environmental harm. Whether nanopesticides, including copper (Cu) formulations, cause reduced levels of toxicity to non-target aquatic organisms is unclear but important to assess. Predicting how aquatic species respond to incidental exposure to Cu-based nanopesticides is challenging because of the expected very low concentrations in the environment, and the two forms of exposure that may occur, namely to Cu ions and Cu nanoparticles. We conducted Cu speciation, tissue uptake, and 7-day toxicity laboratory experiments to test how a model estuarine organism, the amphipod Leptocheirus plumulosus, responded to two popular Cu-based nanopesticides, CuPRO and Kocide, and conventional CuCl2. Exposure concentrations ranged from 0 to 2.5 ppm, which were similar to those found in estuarine water located downstream of agricultural fields. Cu dissolution rates were much slower for the nanopesticides than the ionic formula, and Cu body burden in amphipods increased approximately linearly with the nominal exposure concentration. Amphipod survival declined in a normal dose-response manner with no difference among Cu formulations. Growth and movement rates after 7 days revealed no difference among exposure levels when analyzed with conventional statistical methods. By contrast, analysis of respiration rates, inferred from biomass measurements, with a bioenergetic toxicodynamic model indicated potential for population-level effects of exposure to very low-levels of the two nanopesticides, as well as the control contaminant CuCl2. Our results indicate that toxicity assessment of environmental trace pollutant concentrations may go undetected with traditional ecotoxicological tests. We present a process integrating toxicity test results and toxicodynamic modeling that can improve our capacity to detect and predict environmental impacts of very low levels of nanomaterials released into the environment.

Assuntos

RESUMO

Several studies indicate aluminum (Al) as a potent toxicant, mainly related to central nervous system disorders. However, investigations about the Al effects over salivary glands are still scarce. In this way, the present study aimed to investigate whether the Al chloride (AlCl3) is able of triggering oxidative stress in parotid and submandibular glands of mice and also, if any morphological impairment is observed. For this, twenty mice were divided into two groups: Exposed group (EG), which received 18.5 mg/kg of AlCl3 by intragastric gavage for 60 days and control group (CG), which received distilled water by intragastric gavage during the same period of time. After that, levels of reduced glutathione (GSH) and malonaldehyde (MDA) were analyzed and we performed morphological analyses by evaluating the area of parenchyma, stroma, acini, and ducts in both glands. Statistical analyses were performed by Student's t test and two-way ANOVA, adopting p < 0.05. No abnormal body weight was observed and data indicates that although both major salivary glands are susceptible to Al-induced oxidative stress, by increasing MDA and reducing GSH, only submandibular glands decreased the parenchyma and increased stroma area. Moreover, the submandibular glands showed smaller total area of acini and higher total area of ducts, in comparison with the control group. Notably, AlCl3 induces oxidative stress in both glands, however, submandibular glands showed to be more susceptible to Al effects than parotid glands. Our study gives evidences about Al toxicity in parotid and submandibular glands and claims for new investigations to understand more mechanisms of Al-induced toxicity.

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RESUMO

El cianuro es uno de los tóxicos más peligrosos por su rápida y potente acción, muchas veces letal. Los diferentes tratamientos de la intoxicación tienen su base o explicación en el conocimiento de la toxicocinética y la toxicodinamia. La revisión de la toxicocinética del cianuro muestra que, si bien la vía de la tiosulfato-cianuro sulfotransferasa (rodanasa) es la principal vía metabólica, el complejo con albúmina sérica sería el primer proceso de detoxificación del cianuro en el metabolismo normal. El efecto protector de formadores de cianhidrinas en casos de intoxicación sigue siendo evaluado a nivel experimental. Los estudios actuales sobre la toxicodinamia del cianuro se enfocan en la afinidad de la unión del cianuro al centro binuclear hemo a3-CuB de la citocromo oxidasa en sus diferentes estados redox y enel mecanismo de inhibición de enzimas antioxidantes. Un mayor y mejor entendimiento de la detoxificación del cianuro así como de los mecanismos de acción tóxica podrían llevar al desarrollo de potenciales antídotos.

Cyanide is one of the most dangerous poisons because of its rapid and potent toxicity, most times with lethal outcomes. Different poisoning treatments are based on knowledge of cyanide’s toxicokinetic and toxicodynamic. The review of cyanide’s toxicokinetics shows that, although thiosulfate-cyanide sulfotransferase (rhodanese) is the major metabolic pathway, binding serum albumin would be the first process of detoxification of cyanide in normal metabolism. The protective effect of cyanohydrin formers in cases of poisoning remains experimentally evaluated. Cyanide’s binding affinity to the binuclear center heme a3-CuB of cytochrome oxidase within their different redox states and cyanide’s mechanism of inhibition of antioxidant enzymes are currently still being investigated. More and better understanding of cyanide’s detoxification pathways and/or mechanisms of toxic action could lead to the development of new potential antidotes.

Assuntos

RESUMO

El cianuro es uno de los tóxicos más peligrosos por su rápida y potente acción, muchas veces letal. Los diferentes tratamientos de la intoxicación tienen su base o explicación en el conocimiento de la toxicocinética y la toxicodinamia. La revisión de la toxicocinética del cianuro muestra que, si bien la vía de la tiosulfato-cianuro sulfotransferasa (rodanasa) es la principal vía metabólica, el complejo con albúmina sérica sería el primer proceso de detoxificación del cianuro en el metabolismo normal. El efecto protector de formadores de cianhidrinas en casos de intoxicación sigue siendo evaluado a nivel experimental. Los estudios actuales sobre la toxicodinamia del cianuro se enfocan en la afinidad de la unión del cianuro al centro binuclear hemo a3-CuB de la citocromo oxidasa en sus diferentes estados redox y enel mecanismo de inhibición de enzimas antioxidantes. Un mayor y mejor entendimiento de la detoxificación del cianuro así como de los mecanismos de acción tóxica podrían llevar al desarrollo de potenciales antídotos.(AU)

Cyanide is one of the most dangerous poisons because of its rapid and potent toxicity, most times with lethal outcomes. Different poisoning treatments are based on knowledge of cyanides toxicokinetic and toxicodynamic. The review of cyanides toxicokinetics shows that, although thiosulfate-cyanide sulfotransferase (rhodanese) is the major metabolic pathway, binding serum albumin would be the first process of detoxification of cyanide in normal metabolism. The protective effect of cyanohydrin formers in cases of poisoning remains experimentally evaluated. Cyanides binding affinity to the binuclear center heme a3-CuB of cytochrome oxidase within their different redox states and cyanides mechanism of inhibition of antioxidant enzymes are currently still being investigated. More and better understanding of cyanides detoxification pathways and/or mechanisms of toxic action could lead to the development of new potential antidotes.(AU)

Assuntos