The use of pesticides on crops contributes to the decline of bee populations, and in this sense, bioactive nutrients have been studied to counteract this effect. We suppose that caffeine might be one of these nutrients. We exposed honey bees (Apis mellifera L.) to 0.7 or 2.0 ng/mL imidacloprid, 5.0 μg/mL caffeine in syrup, or 5.0 μg/mL caffeine in syrup plus 0.7 or 2.0 ng/mL imidacloprid. After 72 h, the oxidative status and the food intake were verified. Imidacloprid increased glutathione peroxidase and catalase activities. Caffeine alone or with 2.0 ng/mL imidacloprid also stimulated the activity of glutathione peroxidase but did not alter the effect of the insecticide on the catalase activity. A significant reduction in the concentration of the thiol group of proteins was observed in the two imidacloprid-fed groups, and the addition of caffeine protected these groups. Imidacloprid increased the malondialdehyde concentration while the addition of caffeine partially decreased this effect. Food intake was higher for bees treated with 2.0 ng/mL imidacloprid. Our results show that imidacloprid increased the food intake resulting in oxidative damage, which was partially reversed by caffeine. From these findings, it is inferred that caffeine treatments can be used to mitigate the sublethal effects of this insecticide on honey bees.

BackgroundGossypol is a chemical present in the seeds of cotton plants (Gossypium sp.) that reduces fertility in farm animals. Vitamin E is an antioxidant and may help to protect cells and tissues against the deleterious effects of free radicals. The aim of this study was to evaluate the mechanisms of reproductive toxicity of gossypol in rats and the protective effects of vitamin E. Forty Wistar rats were used, divided into four experimental groups (n = 10): DMSO/saline + corn oil; DMSO/saline + vitamin E; gossypol + corn oil; and gossypol + vitamin E.ResultsFertility was significantly reduced in male rats treated with gossypol in that a significant decrease in epididymal sperm count was observed (P < 0.05) and the number of offspring was significantly reduced in females mated with them (P < 0.05). This dysfunction was prevented by vitamin E. Gossypol caused a significant increase in the activity of the enzymes glutathione peroxidase (P < 0.01) and glutathione reductase (P < 0.01), but vitamin E did not reduce the enzyme activities (P > 0.05). The levels of reduced glutathione and pyridine nucleotides in testis homogenate were significantly reduced by gossypol (P < 0.05 and P < 0.01, respectively) and this reduction was accompanied by increased levels of oxidized glutathione (P < 0.05). Vitamin E showed a preventive effect on the changes in the levels of these substances. Gossypol significantly increased the levels of malondialdehyde (P < 0.01), a lipid peroxidation indicator, whereas treatment with vitamin E inhibited the action of the gossypol. Vitamin E prevented a decrease in mitochondrial ATP induced by gossypol (P < 0.05).ConclusionsThis study suggests that the reproductive dysfunction caused by gossypol may be related to oxidative stress and mitochondrial bioenergetic damage and that treatment with vitamin E can prevent the infertility caused by the toxin.

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There is no use restriction associated with bees for many fungicides used in agriculture; however, this does not always mean that these pesticides are harmless for these nontarget organisms. We investigated whether the fungicide pyraclostrobin, which acts on fungal mitochondria, also negatively affects honey bee mitochondrial bioenergetics. Honey bees were collected from 5 hives and anesthetized at 4°C. The thoraces were separated, and mitochondria were isolated by grinding, filtering, and differential centrifugation. An aliquot of 0.5 mg of mitochondrial proteins was added to 0.5 mL of a standard reaction medium with 4 mM succinate (complex II substrate) plus 50 nM rotenone (complex I inhibitor), and mitochondrial respiration was measured at 30°C using a Clark-type oxygen electrode. Mitochondrial membrane potential was determined spectrofluorimetrically using safranin O as a probe, and adenosine triphosphate (ATP) synthesis was determined by chemiluminescence. Pyraclostrobin at 0 to 50 μM was tested on the mitochondrial preparations, with 3 repetitions. Pyraclostrobin inhibited mitochondrial respiration in a dose-dependent manner at concentrations of 10 μM and above, demonstrating typical inhibition of oxidative phosphorylation. Pyraclostrobin also promoted a decline in the mitochondrial membrane potential at doses of 5 μM and above and in ATP synthesis at 15 μM and above. We conclude that pyraclostrobin interferes with honey bee mitochondrial function, which is especially critical for the energy-demanding flight activity of foraging bees. Environ Toxicol Chem 2020;39:1267-1272. © 2020 SETAC

Silkworm cocoon production has been reduced due to a number of problems other than those inherent in sericulture, such as diseases, malnutrition, and inappropriate management. The use of pesticides in areas surrounding mulberry fields can contaminate these plants and consequently harm caterpillars. The aim of this study was to evaluate whether the application of the fungicide pyraclostrobin in mulberry plants interferes with the mitochondrial bioenergetics and the productive performance of silkworms. Mulberry plants were treated with pyraclostrobin (0, 100, 200, and 300 g ha-1). After 30 d of fungicide application, fifth instar caterpillars were fed with leaves from the treated plants. We evaluated in vitro and in vivo mitochondrial bioenergetics of mitochondria from the head and intestines, as well as the feed intake and mortality rate of the caterpillars and the weight of fresh cocoons and cocoons shells. At doses of 50 µM (in vitro) and 200 g ha-1 (in vivo), pyraclostrobin inhibited oxygen consumption in state 3, dissipated membrane potential, and inhibited ATP synthesis in mitochondria. Pyraclostrobin acted as a respiratory chain inhibitor, affecting mitochondrial bioenergetics. The fungicide did not interfere with food consumption but negatively affected mortality rate and weight of cocoons. Mulberry leaves contaminated with pyraclostrobin negatively impact the mitochondrial bioenergetics of silkworms and cocoon production.