To compare the effects of organic selenium nanoparticles (SeNPs, Se0) and inorganic sodium selenite (NaSe, Na2SeO3, Se4+) on the antioxidant response in maternal and fetal rat liver, pregnant females were treated with two forms of selenium (Se) at equivalent doses during gestation (0.5 mg SeNPs or 0.5 mg NaSe/kg body weight/day). Structural parameters of the liver of gravid females and their fetuses were examined in a sex-specific manner. The oxidative stress parameters superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione S-transferase (GST), total glutathione (GSH) and sulfhydryl groups (SH) were established. In addition, the Se concentration was determined in the blood, liver, urine and feces of the gravid females and in the liver of the fetuses. The structure of the liver of gravid females remained histologically the same after supplementation with both forms of Se, while the oxidative stress in the liver was significantly lower after the use of SeNPs compared to NaSe. Immaturity of fetal antioxidant defenses and sex specificity were demonstrated. This study provides a detailed insight into the differences in the bioavailability of the nano form of Se compared to sodium selenite in the livers of pregnant females and fetuses.

Purpose: This study aimed to investigate the protective effects of gallic acid (GA) against ovarian damage induced by bisphenol A (BPA) exposure in female rats. We evaluated whether GA can mitigate the adverse effects of BPA on ovarian structure, inflammatory markers, oxidative stress, apoptosis, and reproductive hormone levels. Methods: Thirty-two female rats were categorized into four groups: control, GA, BPA, and GA+BPA. Histopathological evaluations of ovarian tissue were performed using hematoxylin-eosin staining. The immunohistochemical analysis was conducted for inflammatory, oxidative DNA damage, and apoptotic markers (Tumor necrosis factor alpha [TNFα], cyclooxygenase-2 [COX2], interleukin-1 beta [IL-1β], 8-hydroxydeoxyguanosine [8-OHdG], and caspase 3). Oxidative stress was assessed by measuring malondialdehyde and superoxide dismutase levels. Furthermore, follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, and progesterone levels were quantified using enzyme-linked immunosorbent assay. Results: Histopathological outcomes revealed that BPA significantly induced follicular degeneration, which was effectively mitigated by GA treatment (P < 0.05). Immunohistochemical analysis highlighted the exacerbation of inflammatory responses and oxidative DNA damage and apoptosis (TNFα, COX-2, IL-1β, 8-OHdG, and caspase 3) in BPA-exposed tissues, which were reduced in the presence of GA (P < 0.05). The assessment of oxidative stress demonstrated that GA could significantly decrease lipid peroxidation and partially restore antioxidant defense mechanisms disrupted by BPA (P < 0.05). Hormonal profiling indicated that BPA exposure altered the levels of FSH, LH, estrogen, and progesterone, with GA treatment showing a capacity to modulate these changes, especially in progesterone levels (P < 0.05). Conclusions: The findings suggest that GA exhibits protective properties against BPA-induced ovarian damage through its antioxidative and anti-inflammatory activities, alongside its ability to modulate hormonal imbalances. This research underscores the therapeutic potential of GA in safeguarding reproductive health against environmental toxicants.

OBJECTIVE: The purpose of this study was to evaluate the effect of carbohydrate loading prior to the cesarean surgery under spinal anesthesia on thiols and ischemia-modified albumin (IMA) levels.
METHODS: Prospective, randomized placebo-controlled study.
METHODS: Seventy-nine pregnant women planned for cesarean sections under spinal anesthesia at Karaman Training and Research Hospital were randomized into a control group (group C) (n = 42), and an oral carbohydrate preloading group (group OCH) (n = 37). OCH loading requires consuming 400 mL the night before surgery and 200 mL up to 2 hours before anesthesia. Group OCH consumed an oral carbohydrate-rich beverage (Nutricia-Fantomalt), and group C consumed an equal volume of water. This study investigated thiol-disulfide homeostasis after preoperative carbohydrate consumption. Preoperative gastric fluid, volume, antral cross-sectional area, hypotension following the birth, and fetal blood gas parameters were compared across groups.
RESULTS: Thiols and IMA levels did not differ across groups before and after surgery (P > .05). Gastric ultrasonography showed similar antral cross-sectional area and stomach volume between groups (P = .172, P = .128, respectively). When surgery caused hypotension, group OCH received more ephedrine for surgery-induced hypotension, although this difference is not statistically significant (P = .704). A clustered error bar (95% confidence interval) plot with an interpolation line was used for a time-based comparison of mean differences in heart rate and mean arterial pressure between the groups.
CONCLUSIONS: This study supports that mothers\' thiols and IMA levels were unaffected by preoperative OCH loading before cesarean surgery. We did not examine thiol and its derivatives in umbilical cord blood; hence, we can not comment on thiol/disulfide homeostasis levels in neonates.

Limited scientific evidence shows that alpha lipoic acid (ALA) can induce regression rates of low-grade squamous intraepithelial lesions (LSILs), but the mechanisms of these effects have not been elucidated. To gain a broader insight into its therapeutic potential and mechanisms of action, the effects of 3 months of supplementation with 600 mg of ALA on antioxidant and lipid status parameters in 100 patients with LSILs were investigated in a randomized, placebo-controlled study. The obtained results are discussed in terms of patients\' initial metabolic status and diet quality (particularly nutritional intake of antioxidants). The obtained results showed that oxidative status biomarkers were not significantly affected by ALA supplementation. However, serum superoxide dismutase (SOD) activity was positively affected in the subgroup of patients with higher dietary antioxidant intake. Surprisingly, ALA supplementation resulted in a small but statistically significant increase in serum low density lipoprotein (LDL), and the observed effect was significantly affected by the initial lipid status of the participants. Larger studies are necessary to gain additional insights on the clinical significance of ALA as an antioxidant and hypolipemic agent and to optimize its potential application in LSIL treatment.

OBJECTIVE: This study aimed to evaluate the hepatotoxicity of buprenorphine in lactating rat pups of buprenorphine-injected mothers. Buprenorphine (BUP), a semisynthetic opioid, is increasingly administrated as a first-line standard maintenance treatment for opioid dependence due to its high safety and efficacy compared to other opioids. Numerous studies have confirmed the safety of BUP maintenance treatment in addicted patients.
OBJECTIVE: This study was designed to assess the effects of BUP on the activities of liver enzymes, oxidative parameters, and liver histopathological changes in pups born to a mother exposed to this drug during lactation.
METHODS: BUP at a dose of 0.5 or 0.1 mg/kg was subcutaneously administrated to lactating rats for 28 days. At the end of the experiment, the pups were anesthetized, and blood samples were obtained from their hearts for measuring liver enzymes. Then the livers of the animals were dissected to measure oxidative stress parameters. In addition, the liver samples were fixed for histopathological evaluation.
RESULTS: The findings indicated a decrease in the activities of serum liver enzymes (ALT and AST) of the pups born to mothers exposed to 0.5 and 1 mg/kg of BUP during lactation. BUP could not change malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels, nor superoxide dismutase (SOD) activity in the liver tissue of animals. Some vacuolated hepatocytes with dark, eccentric nuclei, necrosis with karyolytic nuclei, mitotic figures, and multiple binucleated cells were seen in the pups which received 1 mg/kg of BUP.
CONCLUSIONS: In conclusion, BUP may induce liver dysfunction in pups born to mothers exposed to this drug during lactation.

The aim of this study is to evaluate the effects of scheduled vincristine sulfate therapy on canine oocyte quality and nuclear oocyte maturation, associated with total antioxidant and oxidant status of ovaries and Anti-Müllerian Hormone (AMH) concentrations in dogs with Canine Transmissible Venereal Tumor (CTVT). Six bitches suffering from CTVT and six healthy bitches were included in the study. Hemogram was carried out weekly. AMH measurements and ovariohysterectomy operations were performed after the termination of vincristine sulfate therapies. Tissue samples from ovaries were utilized for Malondialdehyde (MDA), reduced Glutathione (GSH), Superoxide Dismutase (SOD), Total Anti-oxidative Status (TAS), Total Oxidative Status (TOS) measurements, and Oxidative Stress Index (OSI) was calculated. Collected oocytes were evaluated for meiotic competence, after In Vitro Maturation (IVM) and parthenogenetic activation. No difference between the two groups was observed in hematologic parameters (P > 0.05). Meiotic stages of Germinal Vesicle Break Down (GVBD), Metaphase I (MI), and Metaphase II (MII) were significantly different between groups (P < 0.05). The number of oocytes reaching MII and meiotic resumption was lower in the CTVT group. Furthermore, AMH concentrations, oxidant parameters (OSI, TOS, and MDA), and antioxidant parameters (GSH, SOD, and TAS) were also statistically different between groups (P < 0.05). The results of this study show that vincristine sulfate application in the treatment of CTVT could alter oxidant/antioxidant status in ovaries. Apart from these, oocyte quality and IVM rates seem to decline related to gonadotoxicity. Moreover, AMH could be an important marker in the evaluation of oocyte qualities in bitches, as it is in women.

Multi-walled carbon nanotubes (MWCNTs) serve as nanoparticles due to their size, and for that reason, when in contact with the biological system, they can have toxic effects. One of the main mechanisms responsible for nanotoxicity is oxidative stress resulting from the production of intracellular reactive oxygen species (ROS). Therefore, oxidative stress biomarkers are important tools for assessing MWCNTs toxicity. The aim of this study was to evaluate the oxidative stress of multi-walled carbon nanotubes in male rats. Our animal model studies of MWCNTs (diameter ~15-30 nm, length ~15-20 μm) include measurement of oxidative stress parameters in the body fluid and tissues of animals after long-term exposure. Rattus Norvegicus/Wistar male rats were administrated a single injection to the knee joint at three concentrations: 0.03 mg/mL, 0.25 mg/mL, and 0.5 mg/mL. The rats were euthanized 12 and 18 months post-exposure by drawing blood from the heart, and their liver and kidney tissues were removed. To evaluate toxicity, the enzymatic activity of total protein (TP), reduced glutathione (GSH), glutathione S-transferase (GST), thiobarbituric acid reactive substances (TBARS), Trolox equivalent antioxidant capacity (TEAC), nitric oxide (NO), and catalase (CAT) was measured and histopathological examination was conducted. Results in rat livers showed that TEAC level was decreased in rats receiving nanotubes at higher concentrations. Results in kidneys report that the level of NO showed higher concentration after long exposure, and results in animal serums showed lower levels of GSH in rats exposed to nanotubes at higher concentrations. The 18-month exposure also resulted in a statistically significant increase in GST activity in the group of rats exposed to nanotubes at higher concentrations compared to animals receiving MWCNTs at lower concentrations and compared to the control group. Therefore, an analysis of oxidative stress parameters can be a key indicator of the toxic potential of multi-walled carbon nanotubes.

Gastric ulcer is a common gastrointestinal ailment that affects many people worldwide. NSAIDs induced ulcers are the second most common etiology of gastric ulcers. Coconut oil has well-known potential anti-ulcerogenic characteristics. This work aimed to develop and optimize diclofenac potassium (a highly used model drug of NSAIDs) as self-nanoemulsifying delivery system containing coconut oil (DFP-COSNEDS) to overcome its ulcerogenic effect. A mixture design was applied for formula optimization and investigation of the effect of different formulation factors on the droplet size (DS) and polydispersity index (PDI) of the prepared DFP-COSNEDS. The optimized formulae showed good self-emulsification characters and better drug dissolution compared with the drug suspension. The ulcer protection was assessed in-vivo using 7 groups of adult male Wistar rats. Oxidative stress parameters (MDA, GSH, and SOD), inflammatory mediators (PGE-2, TNF-α, and IL-6) and peroxisome proliferator-activated receptor-γ (PPAR-γ) gene expression were measured. The results revealed that pure coconut oil and DFP-COSNEDS containing 25 % of coconut oil showed close figures to normal group and better values than famotidine (FAM) group. In conclusion, coconut oil showed high potential for gastric-protection activity against DFP induced ulcer. DFP-COSNEDS offers dual benefits of improving DFP dissolution and alleviating its ulcerogenic effect.

OBJECTIVE: Berberine is a plant derived alkaloid present in many plants that may has ameliorating potential influences against inflammatory and oxidative conditions. The current study aimed to evaluate the possible protective activity of berberine and investigate its probable mechanisms against sodium nitrite toxicity in the liver.
METHODS: Forty male rats were divided into five groups. Group one, as the control group, received normal saline, group two received berberine (100 mg.kg-1), and group three received sodium nitrite (80 mg.kg-1). Groups four and five received berberine in doses of 50 and 100 mg.kg-1, respectively, and sodium nitrite (80 mg.kg-1) was given orally. All the doses were orally administrated for two months. Then, at the end of the 60th day, the animals were sacrificed, and the liver homogenate was prepared. For evaluating the oxidative injury the levels of albumin (ALB) and aspartate transaminase (AST) in the serum and oxidative stress parameters in the liver were analyzed.
RESULTS: Treatment of rats with sodium nitrite considerably increased the levels of serum AST and liver superoxide anion and significantly reduced the levels of serum ALB, hepatic superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase (CAT) activity in the liver tissue. Berberine treatment could ameliorate all these parameters dose dependently. Berberine at a dose of 100 mg.kg-1 had the best impact and reached the values of oxidative stress parameters to the normal level.
CONCLUSIONS: Our results demonstrated that berberine in a dose-dependent manner offered protection against sodium nitrite-induced oxidative injury in liver, which possibly reflects the antioxidant abilities of this alkaloid.

This study investigated the effect of buprenorphine (BUP) on the livers of pups exposed to this drug during the fetal stage. BUP decreased the activities of serum liver enzymes in exposed animals versus the controls. BUP (0.5 mg/kg) decreased malondialdehyde levels and increased the glutathione levels in the liver of animals versus other groups. The superoxide dismutase activity was elevated in the BUP 0.5 mg/kg group versus the control group. BUP (1 mg/kg) induced histopathological changes in the livers of pups. In conclusion, BUP may induce hepatotoxicity in pups exposed to this drug during the fetal stage.