Bees have a crucial role in pollination; therefore, it is important to determine the causes of their recent decline. Fipronil and imidacloprid are insecticides used worldwide to eliminate or control insect pests. Because they are broad-spectrum insecticides, they can also affect honeybees. Many researchers have studied the lethal and sublethal effects of these and other insecticides on honeybees, and some of these studies have demonstrated a correlation between the insecticides and colony collapse disorder in bees. The authors investigated the effects of fipronil and imidacloprid on the bioenergetic functioning of mitochondria isolated from the heads and thoraces of Africanized honeybees. Fipronil caused dose-dependent inhibition of adenosine 5'-diphosphate-stimulated (state 3) respiration in mitochondria energized by either pyruvate or succinate, albeit with different potentials, in thoracic mitochondria; inhibition was strongest when respiring with complex I substrate. Fipronil affected adenosine 5'-triphosphate (ATP) production in a dose-dependent manner in both tissues and substrates, though with different sensitivities. Imidacloprid also affected state-3 respiration in both the thorax and head, being more potent in head pyruvate-energized mitochondria; it also inhibited ATP production. Fipronil and imidacloprid had no effect on mitochondrial state-4 respiration. The authors concluded that fipronil and imidacloprid are inhibitors of mitochondrial bioenergetics, resulting in depleted ATP. This action can explain the toxicity of these compounds to honeybees.

Abamectin (ABA) is a macrocyclic lactone of the avermectin family used worldwide as an antiparasitic agent in farm animals and pets and as the active ingredient of insecticides and nematicides. In this study, the effects of abamectin on the bioenergetics of mitochondria isolated from rat liver were evaluated. Mitochondria are responsible for converting the energy released by electron transport and stored as the binding energy molecule ATP. Xenobiotics that interfere with its synthesis or utilization can be acutely or chronically toxic. Abamectin (5-25μM) caused concentration-dependent inhibition of the respiratory chain without affecting the membrane potential or the activity of enzymes NADH dehydrogenase or succinate dehydrogenase. This behavior is similar to oligomycin and carboxyatractyloside and suggests direct action on F(o)F(1)-ATPase and/or the adenine nucleotide translocator (ANT). ABA more pronouncedly inhibited ATPase phosphohydrolase activity in intact, uncoupled mitochondria than in freeze-thawed disrupted mitochondria. ADP-stimulated depolarization of the mitochondrial membrane potential was also inhibited by ABA. Our results indicate that ABA interacts more specifically with the ANT, resulting in functional inhibition of the translocator with consequent impairment of mitochondrial bioenergetics. This effect could be involved in the ABA toxicity to hepatocytes.

BackgroundThe liver is an important organ for its ability to transform xenobiotics, making the liver tissue a prime target for toxic substances. The carotenoid bixin present in annatto is an antioxidant that can protect cells and tissues against the deleterious effects of free radicals. In this study, we evaluated the protective effect of bixin on liver damage induced by carbon tetrachloride (CCl4) in rats.ResultsThe animals were divided into four groups with six rats in each group. CCl4 (0.125 mL kg-1 body wt.) was injected intraperitoneally, and bixin (5.0 mg kg-1 body wt.) was given by gavage 7 days before the CCl4 injection. Bixin prevented the liver damage caused by CCl4, as noted by the significant decrease in serum aminotransferases release. Bixin protected the liver against the oxidizing effects of CCl4 by preventing a decrease in glutathione reductase activity and the levels of reduced glutathione and NADPH. The peroxidation of membrane lipids and histopathological damage of the liver was significantly prevented by bixin treatment.ConclusionTherefore, we can conclude that the protective effect of bixin against hepatotoxicity induced by CCl4 is related to the antioxidant activity of the compound.

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Prosopis juliflora, popularly known as Algaroba, is a major problem because the lack of food during the driest times of the year and its high palatability and nutritional value make its fruits (pods) much appreciated by cattle, goats, sheep and other animals. However, the consumption of this plant for long periods can cause a disease called cara-torta (pie face), which is characterized by cranial nerve dysfunction, mainly due to the degeneration and disappearance of neurons in the trigeminal motor nucleus. Algaroba contains piperidine alkaloids that have been suggested as being responsible for its toxicity; one of these alkaloids is juliprosopine. This study was conducted to evaluate the mechanisms of action of juliprosopine in isolated rat brain mitochondria to evaluate the potential mechanisms that lead to neurotoxicity in animals intoxicated by algaroba. Juliprosopine stimulated state-4 respiration at concentrations of 10-25 μM, affected the membrane potential at all concentrations studied (5-25 μM) and affected ATP production only at higher concentrations (15 and 25 μM). Juliprosopine cannot be classified as a member of the protonophoric class of uncouplers, such as 2,4-dinitrophenol or CCCP (m-chlorophenylhydrazone), due to its inability to promote mitochondrial swelling in the hyposmotic medium of potassium acetate. In addition, carboxyatractyloside, Mg(2+), cyclosporine A and dithiothreitol did not protect the uncoupling induced by juliprosopine. Because juliprosopine increased the fluorescence responses of mitochondria labeled with 1-aniline-8-naphthalene sulfonate (ANS) and DPH (1,6-diphenyl-1,3,5-hexatriene), we suggested that its uncoupling action must be attributed to a modification of the arrangement of the inner mitochondrial membrane.