Effects of Boric acid as Maternal Feed Additives on the Development and Sex Ratio of Mouse pups.

Boron is primarily used in industrial applications, with recent interest revolving around its effects on metabolism. In this study, we administered boric acid (BA), which has positive effects on reproduction, in conjunction with feed supplementation to serve as a model for experimental animal development and breeding. The pregnancy performance, offspring development, and biochemical effects of mice given feed supplemented with BA at concentrations of 0 (control group), 250, and 500 ppm (BA groups) were investigated. A total of 18 female Balb-C mice were utilized for pregnancy. The mice were given the BA-supplemented feed during a period encompassing three weeks of pregnancy and three weeks of lactation. The numbers and weights of offspring born in cages on days 19-21 were determined. Blood and tissue samples were collected from the offspring during the third week postnatal, and the malondialdehyde (MDA) and total antioxidant and oxidant status (TAS, TOS, and OSI) levels were determined. A significant increase in female offspring was observed in the groups born to mice fed with BA compared to the control group. Positive development in organ weights was observed in the 250-ppm BA group. The 250-ppm group exhibited a significant increase in TAS compared to the control group, while TOS and MDA levels showed a decrease. Also, the levels of BA groups were found to decrease in both the OSI index serum and organ samples compared to the control group. Thus, the use of 250-ppm BA demonstrated positive effects on female offspring production, organ development, and antioxidant levels.

Protective effect of oxytocin through its anti-inflammatory and antioxidant role in a model of sepsis-induced acute lung injury: Demonstrated by CT and histological findings.

Although several studies demonstrate the anti-inflammatory effect of oxytocin in different pathophysiological processes, there are limited data describing the impact of oxytocin on acute respiratory distress syndrome (ARDS). We aimed to elucidate the protective effect of oxytocin in ARDS with histopathological evaluation and radiological imaging in addition to biochemical markers.Fecal intraperitoneal injection procedure (FIP) was performed on 24 of 32 rats included in the study for creating a sepsis model. Rats were randomly assigned into four groups: control group (no procedure was applied, n = 8), untreated septic group [was operated (FIP) and received no treatment, n = 8], placebo group (FIP, treated with 10 ml/kg of saline at once, n = 8), and treated group (FIP, treated with 0.1 mg/kg of oxytocin at once, n = 8). Chest CT was performed for all rats 20 hours after the procedure and density of the lungs were measured manually by using HU. All animals were sacrificed for histopathological examination of lung damage and blood samples were collected for biochemical analysis.Plasma malondialdehyde (MDA), lactic acid (LA), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), interleukin 1-beta (IL 1-ß) levels were significantly increased in the placebo (FIP + saline) and the untreated (FIP) groups, and plasma levels of all biomarkers were reversed by oxytocin. Further, the density of the lung parenchyma (Hounsfield unit) on CT images and the histopathological lung damage score values were closer to the control group in the oxytocin-treated group compared to the placebo group.Our findings suggested that oxytocin could exert anti-inflammatory, antioxidant and protective effects in FIP-induced ARDS.

Hexagonal boron nitride nanoparticles trigger oxidative stress by modulating thiol/disulfide homeostasis.

BACKGROUND: Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP's dosage and biochemical mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN NPs for the first time. METHODS: hBN NPs at concentrations varying between 50-3200 µg/kg was administered by intravenous injection to Wistar albino rats (n = 80) divided into seven dosage and control groups. Blood and tissue samples were taken after 24 hours. RESULTS: Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dose-dependently. However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically. CONCLUSION: The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by modulating thiol/disulfide homeostasis in rats at higher concentrations.

Investigation of the protective effects of boric acid on ethanol induced kidney injury.

Boric acid (BA) is used as an antioxidant and anti-inflammatory agent, and for regulating mitochondrial membrane potential in many disorders. We investigated the protective effects of BA against chronic ethanol toxicity in rat kidney. We used 32 male rats in four groups of eight: control (C), BA, ethanol (E), and ethanol + BA (E + BA). Kidney samples were taken for histology and biochemistry. Kidney injury was assessed using hematoxylin and eosin (H & E) and periodic acid-Schiff (PAS) staining. TUNEL and caspase-3 immunohistochemistry were used as indicators of apoptosis. We measured biochemical markers of ethanol induced oxidative stress in the kidneys including malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI). The E + BA group TOS, OSI and MDA levels decreased, whereas the TAS level increased compared to group E. Caspase-3 and TUNEL activity in the E + BA group were decreased compared to group E. BA acted as an antioxidant against renal tubule injury caused by chronic use of ethanol. BA protects against apoptosis in renal tubules by decreasing oxidative damage.