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The relationship between DNA damage and repair of peripheral blood leukocytes, liver, kidney and brain cells was investigated in Swiss albino mice (Mas 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 study examined the antioxidative physiological effects of phenolics from an ethanol-water extract of blackthorn flowers orally administrated to C57/BL6 mice for 28 days in daily doses of 25 mg of total phenolics/kg body weight. Contents of phenolics in the intestine, liver, and kidneys collected after 1, 7, 14, 21, and 28 days of extract administration were analyzed by UPLC-MS/MS method. In the same tissues, the antioxidative properties were determined as ferric reducing antioxidant power (FRAP), ABTS•+ scavenging activity, content of reduced glutathione (GSH), and activity of superoxide dismutase (SOD) and catalase (CAT). The lipid peroxidation in tissues was also evaluated by thiobarbituric acid reactive substances (TBARS) assay. The exposed mice (compared to the control ones) had a lower content of TBARS in all tissues mostly on the third/fourth week of daily consumption. SOD activity and GSH content increased on the 28th day in tissues. CAT activity was higher only in the liver after one week of consumption but remained unchanged in other organs throughout the experiment. Phenolic profiles were different in individual tissues. The most prominent increases compared to the control were determined for contents of 3-O-feruloylquinic acid, 4-O-p-coumaroylqiunic acid, kaempferol pentoside, and quercetin rhamnoside in the intestine; for ferulic acid and quercetin 3-O-rutinoside in the liver; and for quercetin 3-O-rutinoside, ferulic acid, and 4-O-p-coumaroylquinic acid in the kidneys. The screened phenolics with different distribution in tissues could be responsible for slight differences in the recorded antioxidative effects.
The aim of this study was to evaluate the genotoxicity of repeated exposure to isoflurane or halothane and compare it with the genotoxicity of repeated exposure to cisplatin. We also determined the genotoxicity of combined treatment with inhalation anaesthetics and cisplatin on peripheral blood leucocytes (PBL), brain, liver and kidney cells of mice. The mice were divided into six groups as follows: control, cisplatin, isoflurane, cisplatin–isoflurane, halothane and cisplatin–halothane, and were exposed respectively for three consecutive days. The mice were treated with cisplatin or exposed to inhalation anaesthetic; the combined groups were exposed to inhalation anaesthetic after treatment with cisplatin. The alkaline comet assay was performed. All drugs had a strong genotoxicity (P < 0.05 vs. control group) in all of the observed cells. Isoflurane caused stronger DNA damage on the PBL and kidney cells, in contrast to halothane, which had stronger genotoxicity on brain and liver cells. The combination of cisplatin and isoflurane induced lower genotoxicity on PBL than isoflurane alone (P < 0.05). Halothane had the strongest effect on brain cells, but in the combined treatment with cisplatin, the effect decreased to the level of cisplatin alone. Halothane also induced the strongest DNA damage of the liver cells, while the combination with cisplatin increased its genotoxicity even more. The genotoxicity of cisplatin and isoflurane on kidney cells were nearly at the same level, but halothane caused a significantly lower effect. The combinations of inhalation anaesthetics with cisplatin had stronger effects on kidney cells than inhalation anaesthetics alone. The observed drugs and their combinations induced strong genotoxicity on all of the mentioned cells.
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