The aim of the present study was to investigate the protective effect of dexpanthenol (Dexp) against cisplatin (Cis)‑induced hepatotoxicity. Thirty‑two Sprague Dawley rats were divided into four groups: Control group (n=8), Dexp group (n=8, 500 mg/kg/ip/daily single dose/3 days Dexp), Cis group (n=8, 7 mg/kg/ip/single dose Cis) and Cis+Dexp group (n=8, 500 mg/kg/ip/daily single dose/3 days Dexp +7 mg/kg/ip/single dose Cis). MDA, CAT, GSH, GSH‑Px, TOS, TAS, OSI, Total Nitrit, IL‑1β, IL‑6 and TNF‑α levels were analyzed in liver tissue samples. After paraffinization of liver tissue samples, histopathological (congestion, loss of glycogen, number of Kupffer cells) and immunohistochemical (caspase‑3 expression) parameters were assessed on the paraffinized liver sections. GSH, TAS, TOS, OSI, Tot Nit, L‑Arginine, ADMA and SDMA levels were measured in the serum samples. Statistically significant differences were found between the groups in terms of all liver tissue biochemical parameters, with the exception of IL‑1β and TNF‑α levels. GSH, CAT, GSH‑Px, TAS and Tot Nit levels were significantly higher in the Cis+Dexp group compared to the Cis group, whereas MDA, TOS, OSI and IL‑6 levels were higher in the Cis group. Similarly, serum GSH, TAS, Tot Nit levels were higher in the Cis+Dexp group whereas TOS, L‑Arginine, ADMA and SDMA levels were higher in Cis group. There were statistically significant differences between Control and Cis groups in terms of congestion increase, increase of glycogen loss, increase of Kupffer cell number and increase of caspase‑3 expression (P<0.001). There was a statistically significant difference between the Cis and the Cis+Dexp groups in terms of histopathologic parameters, with the exception of congestion (P<0.001). To conclude, histopathological, immunohistochemical, and biochemical results of this study demonstrated that Dexp has a protective effect against Cis‑induced hepatotoxicity.

Objectives: The objective of this study is to investigate possible damages to kidney tissues of pregnant rats and their fetuses exposed to acrylamide during pregnancy and possible protective effects of vitamin E against these damages. Material and methods: Rats were randomly assigned to five groups of control, corn oil, vitamin E, acrylamide, vitamin E + acrylamide, six pregnant rats in each. Mother and fetal kidney tissues were examined for malondialdehyde (MDA), reductase glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS), total oxidant status (TOS), urea, creatine, trace elements such as Zn and Cu in the serum and histopathological analyses were conducted. Results: It was determined that acrylamide, administered during pregnancy, statistically significantly increased MDA and TOS levels, maternal serum urea, creatinine, and Zn levels, while it decreased GSH, TAS, SOD, and CAT levels (p ≤ .05) when compared with all other groups in the kidney tissues of pregnant rats and their fetuses and caused tubular degeneration, hemorrhage, narrowing, and closure in Bowman’s space, and, in the E vitamin group, it statistically significantly increased GSH, TAS, SOD, CAT, urea, creatinine, and Zn levels when compared with other groups and lowered TOS and MDA levels to those of the control group (p < .05) and there were no differences between the groups histologically. Conclusion: It was observed that acrylamide administered during pregnancy caused oxidative stress in kidney tissues of mother rats and their fetuses, resulting in tissue damage, and vitamin E application, which is considered to be a powerful antioxidant, inhibited oxidative stress.

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/beta-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.

Background: It has been proven that there is an increase in intestinal permeability in some autoimmune diseases. In our study, we purposed to assess intestinal permeability in vitiligo disease by looking at zonulin levels. At the same time, we aimed to examine the correlation of inflammatory cytokines and lipopolysaccharide (LPS) levels with zonulin.Methods: Forty‐one patients and 41 healthy participants were involved in our study. Blood samples were taken from all patients and controls, and the levels of zonulin, tumor necrosis factor (TNF)‐α, interleukin (IL)‐6 and LPS were examined.Results: The mean of zonulin in the patient group was found to be statistically higher than the control group (p < 0.05). A positive correlation was found between zonulin level and IL‐6, TNF‐α, and LPS levels (p < 0.05). TNF‐α and LPS levels in the vitiligo group were significantly higher than in the control group, but there was no such significance in terms of IL‐6 levels.Conclusion: We think that serum zonulin level increases and intestinal permeability increases in vitiligo disease.