Despite the excellent chemotherapeutic effect of irinotecan, its cytotoxicity and genotoxicity in normal cells remains a major problem in chemotherapy. This study was carried out to find whether propolis preparations and related flavonoids (quercetin, naringin) might enhance irinotecan-induced cytotoxicity to tumor cells in mice bearing Ehrlich ascites tumors (EAT) while protecting normal blood, liver, and kidney cells. The preparation of propolis and their flavonoids were given to mice intraperitoneally at a dose of 100 mg kg(-1) body weight for three consecutive days before the ip injection of EAT cells (2×10(6)). Irinotecan was administered ip at dose of 50 mg kg(-1) on days 3, 4, and 5 after tumor cell inoculation. The combination treatment resulted in substantial inhibition of the growth of EAT cells as well as treatment with quercetin or irinotecan alone, whereas other treatment by itself showed little effect. However, when mice were pre-treated with test components prior to irinotecan, the frequencies of irinotecan-induced micronuclei (MN) was decreased but in mice bearing tumor QU and EEP increased number of micronucleated cells. Propolis preparation and related flavonoids were found to exhibit an important immunomodulatory effect and could decrease irinotecan-induced toxic and genotoxic effects to normal cells without effecting irinotecan cytotoxicity in EAT cells.
Body size has a pervasive effect on animal functioning and life history with size dependent changes in performance and physiology throughout ontogeny being common in many ectothermic vertebrates. However, as selection on juvenile life history stages is strong, juveniles often offset the disadvantages of small body size by disproportionate levels of performance. Here, we investigate size-related changes in defensive strike performance in an arboreal pit viper, Trimerusurus (Cryptelytrops) albolabris. Our data show a significant negative allometry in the scaling of head dimensions and head mass to body mass. However, strike velocity and strike distance are independent of body mass, with juveniles in our sample striking as fast and as far as adults. In contrast to model predictions suggesting that acceleration capacity should decrease with increasing body mass, acceleration capacity increases with snake body mass. Our results suggest that this is the result of a negative allometric scaling of head mass combined with an isometric scaling of the dorsal epaxial musculature. Finally, our data show a significant sexual dimorphism in body size and strike velocity with females being heavier and striking faster independent of the dimorphism in body size.
These results suggest that the dietary flavonoids could reduce retinoic acid-induced oxidative stress and bone loss and that flavonoids may be useful therapeutics for prevention of skeletal diseases.
The aim of this study was to assess radioprotective effects of quercetin and the ethanolic extract of propolis (EEP) in CBA mice exposed to a single radiation dose 4 Gy ( 60 Co). The mice were treated with 100 mg kg -1 quercetin or EEP a day for three consecutive days either before (pre-treatment) or after gamma-irradiation (therapy). Leukocyte count was determined in blood drawn from the tail vein, and DNA damage in leukocytes was assessed using the alkaline comet assay. Genotoxic effects of the test compunds were also evaluated in non-irradiated mice. The levels of radioprotection provided by both test compounds were compared with those established in mice that were given chemical radioprotector S-(2-Aminoethyl)isothiouronium bromide hydrobromide (AET). Mice that received pre-treatment were less sensitive to irradiation. Mice given the post-irradiation therapy showed a slight but not signifi cant increase in total leukocyte count over irradiated negative control. Quercetin showed better protective properties than EEP in both pre-treatment and therapy, and activated a higher number of leukocytes in non-irradiated mice. The alkaline comet assay suggests that both natural compounds, especially when given as pre-treatment, protect against primary leukocyte DNA damage in mice. At tested concentrations, EEP and quercetin were not genotoxic to non-irradiated mice. AET, however, caused a slight but not signifi cant increase in DNA damage. Although the results of this study show the radioprotective potential of the test compounds, further investigation is needed to clarify the underlying protection mechanisms.
Bite force is a key performance trait in lizards because biting is involved in many ecologically relevant tasks, including foraging, fighting and mating. Several factors have been suggested to impact bite force in lizards, such as head morphology (proximate factors), or diet, intraspecific competition and habitat characteristics (ultimate factors). However, these have been generally investigated separately and mostly at the interspecific level. Here we tested which factors drive variation in bite force at the population level and to what extent. Our study includes 20 populations of two closely related lacertid species, Podarcis melisellensis and Podarcis sicula, which inhabit islands in the Adriatic. We found that lizards with more forceful bites have relatively wider and taller heads, and consume more hard prey and plant material. Island isolation correlates with bite force, probably by driving resource availability. Bite force is only poorly explained by proxies of intraspecific competition. The linear distance from a large island and the proportion of difficult-to-reduce food items consumed are the ultimate factors that explain most of the variation in bite force. Our findings suggest that the way in which morphological variation affects bite force is species-specific, probably reflecting the different selective pressures operating on the two species.
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.
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