RESUMEN
Objective: The aim of this study was to investigate the effect of various astaxanthin (ATX) doses on oxidative damage and autophagy in renal ischemia-reperfusion (I/R) injury-modeled rats. Methods: The rats were divided into five groups: sham group (n=8), I/R (n=8), I/R + 5 mg/kg ATX (n=8), I/R + 10 mg/kg ATX (n=8), and I/R + 25 mg/kg ATX (n=8) groups. ATX was dissolved in 5 mg/kg, 10 mg/kg, and 25 mg/kg olive oil for 7 days and administered to the rats in the experimental group. Sham and I/R groups were also administered ATX solution (olive oil) via oral gavage for 7 days. Renal ischemia reperfusion was induced in all rats except the sham group after the last dose was administered on the 7th day. Reperfusion was conducted for 24 hours after 45 minutes of ischemia. Results: Blood samples were collected, and kidney tissue were incised for biochemical and histological analyses. Superoxide dismutase (SOD) and total antioxidant status (TAS) were significantly lower in the I/R group than in the sham group (p<0.05), whereas malondialdehyde (MDA) and total oxidant status (TOS) values were higher (p<0.05). It was determined that SOD and TAS increased and MDA and TOS decreased in the ATX-administration groups compared with the I/R group, independent of the dose (p<0.05). In the 25 mg/kg ATX + I/R group, Beclin-1 and LC3ß immunoreactivities were significantly higher than those in the other groups (p<0.05). The lowest p62 immunoreactivity was observed in the 25 mg/kg ATX + I/R group. Conclusions: ATX had a protective effect on kidney function and against oxidative damage. Furthermore, high-dose ATX administration protected kidney tissue via autophagy induction in this study.
RESUMEN
We investigated the effects of acrylamide (AA) and vitamin E treatment during pregnancy on brain tissues of fetuses and on adult rats. Pregnant rats were divided into five groups: control, corn oil, vitamin E, AA, vitamin E +AA. The rats administered AA received10 mg/kg/day and those administered vitamin E received 100 mg/kg/day both by via oral gavage for 20 days. On day 20 of pregnancy, half of the pregnant rats were removed by cesarean section in each group. Morphological development parameters were measured in each fetus and histopathological, biochemical and genetic analyses were conducted on the fetuses. The remaining pregnant rats in each group gave birth to the fetuses vaginally and biochemical, histopathological, genetic and cognitive function tests were conducted when the pups were 8 weeks old. AA administration caused adverse effects on fetus number, fetal weight, crown-rump length, placenta and brain weight. AA negatively affected malondialdehyde, reduced glutathione, total oxidant and antioxidant status, brain derived neurotrophic factor (BDNF) levels, brain tissue morphology, histopathology error score and gene expression (BDNF/ß-actin mRNA ratio) in fetuses. AA administration caused disruption of biochemical, histopathological and cognitive functions in adult rats. Vitamin E provided protection against neurotoxicity in both fetuses and adult rats. We conclude that exposure to AA during pregnancy should be avoided and adequate amounts of antioxidants, such as vitamin E, should be consumed.
