Ochratoxin A (OTA) and citrinin (CTN) are nephrotoxic mycotoxins often found together in grain. The aim of this study was to measure their accumulation in the kidney and liver of adult male Wistar ...rats, see how it would be affected by combined treatment, and to determine if resveratrol (RSV) would decrease their levels in these organs. The rats received 125 or 250 mg/kg bw of OTA by gavage every day for 21 days and/or 20 mg/kg bw of CTN a day for two days. Two groups of rats treated with OTA+CTN were also receiving 20 mg/kg bw of RSV a day for 21 days. In animals receiving OTA alone, its accumulation in both organs was dose-dependent. OTA+CTN treatment resulted in lower OTA but higher CTN accumulation in both organs at both OTA doses. RSV treatment increased OTA levels in the kidney and liver and decreased CTN levels in the kidney. Our findings point to the competition between CTN and OTA for organic anion transporters 1 and 3.
This study aimed to explore involvement of oxidative stress in sterigmatocystin (STC) toxicity in male Wistar rats. Animals were orally treated with a single STC dose (10, 20 and 40 mg/kg b.w.). ...Short-term treatment resulted in moderate oxidative stress determined by a significant increase of malondialdehyde (MDA; all STC doses) and catalase (CAT; 10 mg/kg b.w.) in plasma, a decrease of glutathione peroxidase (GPx; 20 and 40 mg/kg b.w.) in the liver, and increase of MDA and superoxide dismutase (SOD) in kidneys (all STC doses). Heat shock protein (Hsp27 and Hsp70) expression was determined by Western blotting in rat liver and kidneys. Hsp27 expression was downregulated by STC, particularly in the liver (40 mg/kg b.w.). The lowest STC dose elevated the expression of Hsp70 in both liver and kidneys, while an increase in STC doses restored Hsp70 expression to control. Alterations in expressions of Hsp27 and Hsp70 could be only partially associated with oxidative stress. STC provoked a significant DNA damage in both liver and kidneys (alkaline comet assay), but the liver was more affected by a broader spectrum of DNA lesions. Oxidative DNA damage (hOGG1-modified comet assay) contribute to the overall mechanism of STC-induced DNA damage in both organs, but kidneys in general seem to be more susceptible to oxidative stress upon short-term exposure to sublethal doses of STC.
The original version of this article unfortunately contained a mistake. The author’s first and last names were interchanged in the published version of this article. The corrected author names are ...given in this article.
Humans have used insecticides since ancient times. The spectrum and potency of available insecticidal substances has greatly expanded since the industrial revolution, resulting in widespread use and ...unforeseen levels of synthetic chemicals in the environment. Concerns about the toxic effects of these new chemicals on non-target species became public soon after their appearance, which eventually led to the restrictions of use. At the same time, new, more environmentally-friendly insecticides have been developed, based on naturally occurring chemicals, such as pyrethroids (derivatives of pyrethrin), neonicotinoids (derivatives of nicotine), and insecticides based on the neem tree vegetable oil (
), predominantly azadirachtin. Although these new substances are more selective toward pest insects, they can still target other organisms. Neonicotinoids, for example, have been implicated in the decline of the bee population worldwide. This review summarises recent literature published on non-target toxicity of neonicotinoids, pyrethroids, and neem-based insecticidal substances, with a special emphasis on neonicotinoid toxicity in honeybees. We also touch upon the effects of pesticide combinations and documented human exposure to these substances.
The aim of this study was to investigate the genotoxic potential of low doses of chlorpyrifos (CPF) on blood and bone marrow cells in adult male Wistar rats. CPF was administered by oral gavage at ...daily doses of 0.010, 0.015, and 0.160 mg/kg of body weight (bw) for 28 consecutive days. Positive control (PC) was administered 300 mg/kg bw/day of ethyl methane sulphonate (EMS) for the final three days of the experiment. Toxic outcomes of exposure were determined with the
micronucleus (MN) assay and alkaline comet assay. The 28-day exposure to the 0.015 mg/kg CPF dose, which was three times higher than the current value of acute reference dose (ARfD), reduced body weight gain in rats the most. The
MN assay showed significant differences in number of reticulocytes per 1000 erythrocytes between PC and negative control (NC) and between all control groups and the groups exposed to 0.015 and 0.160 mg/kg bw/day of CPF. The number of micronucleated polychromatic erythrocytes per 2000 erythrocytes was significantly higher in the PC than the NC group or group exposed to 0.015 mg/kg bw/day of CPF. CPF treatment did not significantly increase primary DNA damage in bone marrow cells compared to the NC group. However, the damage in bone marrow cells of CPF-exposed rats was much higher than the one recorded in leukocytes, established in the previous research. Both assays proved to be successful for the assessment of CPFinduced genome instability in Wistar rats. However, the exact mechanisms of damage have to be further investigated and confirmed by other, more sensitive methods.
DNA damage in the liver and kidney cells of adult male Wistar rats was studied using the comet assay after a 28-day oral administration of tembotrione at doses of 0.0007, 0.0013 and 0.7 mg/kg ...b.w./day AOEL (acceptable operator exposure level), REL (residual exposure level) and 1000× AOEL. As a descriptor of DNA damage, tail intensity was used. Antioxidant status was assessed by activity of glutathione peroxidase (GPx). Significant DNA damage was recorded in the kidney cells at all three doses as compared to negative control. In parenchymal liver cells, significant DNA damage was observed in AOEL and 1000× AOEL doses, while in non-parenchymal liver cells, only AOEL-treated group was significantly different compared to negative control. In both types of liver cells, REL and 1000× AOEL doses were significantly different from the AOEL dose. No significant changes in GPx activity compared to control were observed at any exposure level. The results of the present study suggest that repeated in vivo exposure to tembotrione led to low-level DNA instability in kidney and liver cells. Exposure to the highest tembotrione dose showed a relatively weak response with the alkaline comet assay. Further research should focus on the effects of this herbicide in other models along with different exposure scenarios.
The freshwater water flea (Daphnia magna Straus, 1820) is prey for numerous predators. Yet it possesses a wide range of strategies to defend itself against predation. The aim of this work is to ...investigate the defensive mechanisms employed by D. magna to reduce predation by the coelenterate Hydra viridissima, and two planarians, Polycelis felina and Dugesia gonocephala. To do this, we used a freshwater microcosm. An additional aim is to investigate interactions with the presence of the isolated endosymbiotic algae from green hydra, thus combining and observing the interaction of the zooplankton and microalgal component. Each experiment included five replicates (13.5 °C, 25 °C), in crystallizing glass containers (60 mL volume, 60 mm diameter, 35 mm height), including satiated (fed with larvae of Artemia salina) and starved predators, respectively (one or five individuals of a particular predator species in one microcosm). As the isolated microalgae are unique, we tracked the following three mechanisms of Daphnia defense for the first time including precisely this microalgal component: (i) grouping (visual magnification), i.e., two or more Daphnia holding together; (ii) the phenomenon of overproduction, i.e., any number of Daphnia in one container above the 10 initially added individuals; and (iii) accelerated movement (“bullet movement”), i.e., high-speed movements in particular microcosms. The results provide new information for a better understanding of the interspecific relationships in systems that include both zooplankton and microalgal components.
The aim of this study was to establish the involvement of calcium signalling in genotoxicity, apoptosis and necrosis evoked by ochratoxin A (OTA) and citrinin (CTN) alone or in combination in porcine ...kidney PK15 cells. Cell proliferation test (MTT) and trypan blue assays (24 h) demonstrated that CTN (IC
50
= 73.5 ± 1.0, 75.4 ± 1.4 μM, respectively) was less toxic than OTA (IC
50
= 14.0 ± 2.4, 20.5 ± 1.0 μM, respectively). To test their cytotoxic interactions, two doses of single OTA (6 and 10 μM) and CTN (30 and 50 μM) and their combinations were applied. Combined treatment showed additive cytotoxic effects. OTA and CTN induced dose-dependent increase in cytosolic calcium level (assessed with Fura-2 AM). However, combined treatment did not provoke additional increase in calcium signal. The rate of apoptosis and necrosis (DAPI-antifade staining) was significantly higher after 12 h than 24 h, while the frequencies of micronuclei (MNs) and nuclear buds (NBs) were higher after 24 h than 12 h treatment. Combined exposure resulted in apoptotic and necrotic synergism, while genotoxic effects of OTA + CTN were noted as antagonistic or additive. Co-exposure of cells to calcium chelator BAPTA-AM significantly reduced CTN and OTA + CTN-evoked apoptosis. Twenty-four hour after co-exposure to BAPTA-AM and a single OTA and CTN, MNs significantly decreased while NBs dropped significantly after co-treatment with BAPTA-AM and OTA + CTN. In conclusion, disturbance of Ca
2+
homeostasis caused by OTA and CTN plays a significant role in cell genotoxicity and death.
Imidacloprid is a neonicotinoid insecticide that acts selectively as an agonist on insect nicotinic acetylcholine receptors. It is used for crop protection worldwide, as well as for non-agricultural ...uses. Imidacloprid systemic accumulation in food is an important source of imidacloprid exposure. Due to the undisputable need for investigations of imidacloprid toxicity in non-target species, we evaluated the effects of a 28-day oral exposure to low doses of imidacloprid (0.06 mg/kg b. w./day, 0.8 mg/kg b. w./day and 2.25 mg/kg b. w./day) on cholinesterase activity, oxidative stress responses and primary DNA damage in the blood and brain tissue of male Wistar rats. Exposure to imidacloprid did not cause significant changes in total cholinesterase, acetylcholinesterase and butyrylcholinesterase activities in plasma and brain tissue. Reactive oxygen species levels and lipid peroxidation increased significantly in the plasma of rats treated with the lowest dose of imidacloprid. Activities of glutathione-peroxidase in plasma and brain and superoxide dismutase in erythrocytes increased significantly at the highest applied dose. High performance liquid chromatography with UV diode array detector revealed the presence of imidacloprid in the plasma of all the treated animals and in the brain of the animals treated with the two higher doses. The alkaline comet assay results showed significant peripheral blood leukocyte damage at the lowest dose of imidacloprid and dose-dependent brain cell DNA damage. Oral 28-day exposure to low doses of imidacloprid in rats resulted in detectable levels of imidacloprid in plasma and brain tissue that directly induced DNA damage, particularly in brain tissue, with slight changes in plasma oxidative stress parameters.
Display omitted
•Male Wistar rats were orally exposed to low doses of imidacloprid for 28 days.•Detectable levels of imidacloprid were found in plasma and brain tissue.•Imidacloprid induced slight changes in oxidative stress parameters.•Primary DNA damage was dose-dependent in brain cells.
PDF
