Form-function relationships underlie rapid dietary changes in a lizard.

Macroevolutionary changes such as variation in habitat use or diet are often associated with convergent, adaptive changes in morphology. However, it is still unclear how small-scale morphological variation at the population level can drive shifts in ecology such as observed at a macroevolutionary scale. Here, we address this question by investigating how variation in cranial form and feeding mechanics relate to rapid changes in diet in an insular lizard (Podarcis siculus) after experimental introduction into a new environment. We first quantified differences in the skull shape and jaw muscle architecture between the source and introduced population using three-dimensional geometric morphometrics and dissections. Next, we tested the impact of the observed variation in morphology on the mechanical performance of the masticatory system using computer-based biomechanical simulation techniques. Our results show that small differences in shape, combined with variation in muscle architecture, can result in significant differences in performance allowing access to novel trophic resources. The confrontation of these data with the already described macroevolutionary relationships between cranial form and function in these insular lizards provides insights into how selection can, over relatively short time scales, drive major changes in ecology through its impact on mechanical performance.

DNA damage and repair after exposure to sevoflurane in vivo, evaluated in Swiss albino mice by the alkaline comet assay and micronucleus test.

The relationship between DNA damage and repair of peripheral blood leukocytes, liver, kidney and brain cells was investigated in Swiss albino mice (Mus musculus L.) after exposure to sevoflurane (2.4 vol% for 2 h daily, for 3 days). Genetic damage of mouse cells was investigated by the comet assay and micronucleus test. To perform the comet assay, mice were divided into a control group and 4 groups of exposed mice sacrificed on day 3 of the experiment, at 0, 2, 6 or 24 h after the last exposure to sevoflurane. Mean tail length (TL), tail moment (TM), and tail intensity (TI) values were significantly higher in exposed mice (all examined organs) than in the control group. Significant DNA damage immediately after exposure to sevoflurane was observed in leukocytes. Damage induction in the liver, kidney, and brain occurred 6 h later than in leukocytes, as expected according to the toxicokinetics of the drug, where blood is the first compartment to absorb sevoflurane. However, none of the tested tissues revealed signs of repair until 24 h after the exposure. To distinguish the unrepaired genome damage in vivo, the micronucleus test was applied. Number of micronuclei in reticulocytes showed a statistically significant increase, as compared with the control group at all observed times after the treatment.

The effects of prometryne on subchronically treated mice evaluated by SCGE assay.

Prometryne is a methylthio-s-triazine herbicide used to control annual broadleaf and grass weeds in many cultivated plants. Significant traces are documented in environment, mainly water, soil and plants used for human and domestic animal nutrition. Data on the toxic effects of prometryne and other methylthio-s-triazine have scorcely been published. The goal of this study was to investigate if prometryne, applied orally, could induce DNA damage in mouse leukocytes, in subchronical in vivo experimental design. Three different doses of prometryne were applied per os repeatedly every 48 hours. After the 7th dose (day 14) and the 14th dose (day 28) blood leucocytes were analyzed by alkaline Single Cell Gel Electrophoresis (Comet) assay. The results of three different comet parameters showed general increase in Olive tail moment, tail length and tail intensity values in treated groups of animals. The increase in measured values was almost proportional to the dose received and the time of exposure. We conclude that prometryne or its metabolic residues have the potential to induce processes that cause genotoxic effects on leukocytes on mice in in vivo repeated exposure.

Carbendazim combined with imazalil or cypermethrin potentiate DNA damage in hepatocytes of mice.

Traces of pesticides imazalil, cypermethrin and carbendazim are detected in plants used for human consumption. To explore whether their application in oral combinations will induce DNA breaks in hepatocytes, a subchronic in vivo experiment was performed in Swiss mice. Doses of 10 mg kg(-1) of imazalil (im) and cypermethrin (cy), and 20 mg kg(-1) of carbendazim (car) and their combinations (im, 10 mg kg(-1) + cy, 10 mg kg(-1); im, 10 mg kg(-1) + car, 20 mg kg(-1); car, 20 mg kg(-1) + cy, 10 mg kg(-1)) were applied daily for 28 days. Afterward, DNA damage in hepatocytes was evaluated by comet assay. Individually, imazalil and cypermethrin damaged DNA at alkali-labile sites, while the tail moment (TM) of carbendazim alone was similar to control but with higher tail length. In combination with carbendazim clastogen, properties of imazalils and cypermethrins were potentiated compared to all other treatments and control. There were pronounced sex differences in pattern of fragmentation between treated groups. Higher long tail nuclei (LTN) in females indicate that certain cells in females were especially prone to total nucleus disintegration. Due to synergistic effects, low environmentally present concentrations of imazalil and cypermethrin in food, and especially their mixtures with carbendazim have genotoxic potential that could be particularly dangerous over prolonged exposure in mammalian organism.

Radioprotective effects of propolis and quercetin in gamma-irradiated mice evaluated by the alkaline comet assay.

The radioprotective effects of ethanolic extract of propolis (EEP) and quercetin on the white blood cells of the whole-body irradiated CBA mice were investigated. Irradiation was performed using a gamma-ray source ((60)Co), and absorbed dose was 9 Gy. The efficiency of test components was evaluated when given intraperitoneally (ip) at a dose of 100 mg kg(-1) for 3 consecutive days before and/or after irradiation. Moreover, possible genotoxic effects of test components were also assessed on non-irradiated animals. For each experimental group leukocyte count was determined and the primary DNA damage in leukocytes was assessed using the alkaline comet assay. The higher efficiency of EEP and quercetin was observed when given preventively. The results suggest that propolis and quercetin given to mice before irradiation protect their white blood cells from lethal effects of irradiation and diminish primary DNA damage as confirmed by the alkaline comet assay. Positive results obtained on gamma-irradiated mice given EEP and quercetin, complementary with our earlier observations on survival of irradiated mice, indicate that these compounds could be considered effective non-toxic radioprotectors. The exact mechanisms of radioprotection by these compounds and their effects on DNA repair processes are still to be elucidated.