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Abstract Background Bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC) present serious reproductive health risks and management challenges, with poor control attributed to survival of treatment-resistant biofilm communities. Boric acid is used in various regimens for non-albicans VVC and recurrent BV. We investigated safety and efficacy of a novel boric acid–based vaginal anti-infective with enhanced antibiofilm activity (TOL-463) in treating BV and VVC. Methods In this phase 2 randomized, investigator-blinded trial conducted at 2 sexual health clinics, women with BV or VVC were randomly assigned (1:1) to 7 nights of TOL-463 vaginal gel or insert. The primary test of cure (TOC) was clinical cure at day 9–12; safety was assessed at TOC and day 21–30. Results One hundred six participants (53 with BV, 36 VVC, 17 both) were enrolled; most were African American (69%). Clinical cure rate of BV at TOC was 59% (95% confidence interval [CI], 41%–75%) for TOL-463 insert and 50% (95% CI, 31%–69%) for TOL-463 gel, and for VVC, 92% (95% CI, 67%–99%) for TOL-463 insert and 81% (95% CI, 57%–93%) for TOL-463 gel. Both products were safe and well tolerated with no secondary cases of VVC; vulvovaginal burning was the most common adverse event (9.6%). Conclusions TOL-463, especially in vaginal insert form, is effective and safe in treating BV and VVC. Future studies should assess the potential role of TOL-463 as a biofilm disrupter in enhancing likelihood of cure relative to approved therapies, reducing recurrence rates, and combined with traditional antimicrobials. Clinical Trials Registration NCT02866227. TOL-463 vaginal gel or insert, a boric acid–based anti-infective with enhanced antibiofilm activity, was effective and safe in treating Bacterial Vaginosis and Vulvovaginal Candidiasis, with the vaginal insert demonstrating higher efficacy for both conditions.

Ischemia/reperfusion (I/R) injury is associated with a strong inflammatory and oxidative stress response to hypoxia and reperfusion that impair organ function. We aimed to investigate the role of oxidative stress, renal inflammation, and apoptosis in the injury of the kidney tissue after ischemic reperfusion, and the protective effect of dose-dependent boric acid administration. For this purpose, 35 Sprague Dawley albino rats were divided into five groups of seven animals in each group: Sham, I/R and I/R + boric acid (BA) (i.p at doses of 50, 100, and 200 mg/kg). All animals underwent nephrectomy (the right kidney was removed) and were expected to recover for 15 days. After recovery, each animal received 45 min of ischemia. BA was injected intraperitoneally 10 min before reperfusion and a 24-h reperfusion procedure was performed. Sham group only underwent surgical stress procedure. In order to investigate the oxidative stress induced by I/R injury and antioxidant effects of different BA doses in the kidney tissue, TAS, TOS, MDA, SOD, CAT, and GSH levels were measured. DNA fragmentation, cytochrome C levels, caspase 3 activity were measured to determine apoptotic index in tissue. IL-6 and TNF-α levels were measured in the evaluation of inflammation. Hematoxylin-eosin and TUNEL staining was performed for histopathological examinations. As a result, increased oxidative stress, inflammation, and apoptosis after I/R were decreased with different doses of BA treatment. The application of high-dose BA was found to be lower in anti-apoptotic, anti-inflammatory, and antioxidant effects than in the low-dose groups.

Background Boric acid is an important alternative to antibiotics due to its positive effects on the immune system, endocrine system, lipid metabolism, mineral metabolism and energy metabolism. Different doses of boric acid supplemented to diet and water may influence performance, hatchability and intestinal bacterial load in Japanese quails with various feather colours. Objective The aim of the study was to determine the effects of different doses of boric acid, supplemented in feed and water, on performance, hatchability and intestinal bacterial load in Japanese quails with different feather colours. Methods A completely randomized 5 × 4 factorial design was implemented, consisting of five dietary treatments and four feather colour groups. The dietary treatments were control (basal diet without supplementation), F100 (100 mg/kg boric acid added to feed), F300 (300 mg/kg boric acid in feed), W100 (100 mg/L boric acid added to drinking water) and W300 (300 mg/L boric acid in water). A total of 300 Japanese quails (Coturnix coturnix japonica) with different feather colour genotypes—yellow (Y), white (W), grey (G) and black (B)—served as the experimental subjects. Each treatment group included 60 quails, with 15 individuals from each feather colour and experiment lasted for 90 days. Results Supplementation of boric acid to feed and water did not affect egg production, feed consumption, feed conversion rate, viability or water consumption (p > 0.05). In the F300 group, hatchability from set eggs (p < 0.05) and from fertile eggs (p < 0.01) increased, whereas embryo mortality decreased significantly (p < 0.01). Compared to the control, total lactic acid bacteria count increased and coliform bacteria count decreased significantly in boric acid‐supplemented groups (F300, W100 and W300) (p < 0.001). Egg production, feed conversion rate, viability, hatchability and intestinal bacterial load were similar among different feather colour varieties (p > 0.05). Feed consumption was highest in yellow and grey genotypes (p < 0.001). Conclusion Boric acid can be used as a feed supplementation with positive effects on hatchability performance and intestinal health. Quail genotypes were generally similar in terms of the examined features. This study aimed to evaluate the effects of different dietary and water‐supplemented doses of boric acid on performance, hatchability, and intestinal bacterial load in Japanese quails of various feather colour genotypes. Boric acid supplementation improved hatchability rates and beneficially modulated intestinal microbiota without impairing production traits, supporting its use as a functional feed additive.

This study evaluated the antioxidant, anti-inflammatory, and anti-fibrotic effects of boric acid-functionalized bentonite nanostructures (BABTs) in a rat model of paraquat (PQ)-induced pulmonary toxicity, a well-established model for herbicide-related lung fibrosis. BABTs (20-60 nm) were synthesized via a microwave-assisted technique, characterized by dynamic light scattering, scanning electron microscopy, Fourier-transform infrared, and ultraviolet-visible spectroscopy, confirming PQ-BABT complex formation. Forty-eight male Wistar rats were randomized into eight groups (n = 6/group): negative control (saline), positive control (single 100 mg/kg PQ oral dose), and experimental groups receiving BABTs or boric acid (BA) at 10, 50, or 100 mg/kg/day orally, 30 min post-PQ. After 14 days, lung malondialdehyde (MDA) levels and histopathological changes (H&E, Masson's Trichrome) were assessed. BABTs at 50 mg/kg significantly decreased lung malondialdehyde (MDA) levels (P < 0.05) and significantly attenuated tissue injury (P < 0.05), suggesting an attenuation of oxidative stress, inflammation, and fibrosis, while boric acid (BA) demonstrated no significant effect. BABTs mitigate PQ-induced lung injury through antioxidant, anti-inflammatory, and anti-fibrotic mechanisms, enhanced by reducing PQ bioavailability. These findings position BABTs as a promising therapeutic candidate for PQ-induced pulmonary fibrosis, warranting further clinical evaluation.

Background Boric acid (BA) is found in various household products. Paediatric intoxication via unusual routes remains a concern. This case report describes an 8-year-old boy who ingested BA through contaminated pasta water, with documented blood and urine boron levels. Case presentation An 8-year-old boy consumed homemade pasta prepared with water inadvertently contaminated with a 3% BA solution (estimated intake: 2.7–8.1 g). He presented with nausea and abdominal pain. On admission, routine blood and urine analyses revealed normal creatinine and urea levels. He was admitted for observation, intravenous fluid therapy, and monitoring of boron levels. The patient experienced one episode of vomiting and headache, which resolved with acetaminophen. Serial blood and urine boron levels were measured. The patient’s initial plasma boron concentration was 16.5 mg/L, decreasing significantly within 24 h, consistent with BA’s pharmacokinetics. Despite the estimated BA intake, the patient remained largely asymptomatic after the initial episode. Follow-up tests one-month post-discharge were normal. Conclusions This case highlights the potential for accidental BA ingestion in children and emphasizes the importance of prompt recognition and supportive treatment with intravenous fluids. While blood boron levels can confirm exposure and elimination, correlation with clinical manifestations requires further study. Ingestion of BA doses exceeding 3 g warrants immediate hyperhydration and monitoring. BA is readily absorbed, with renal excretion being the primary route of elimination. Prompt hydration is crucial. A one-month follow-up with clinical evaluation and renal function tests appears sufficient for asymptomatic patients. Further research is needed to better define the toxic dose of BA and its clinical correlation.

Summary Boron (B) deficiency is one of the major causes of growth inhibition and yield reduction in Brassica napus (B. napus). However, the molecular mechanisms of low B adaptation in B. napus are largely unknown. Here, fifty‐one BnaWRKY transcription factors were identified as responsive to B deficiency in B. napus, in which BnaAn.WRKY26, BnaA9.WRKY47, BnaA1.WKRY53 and BnaCn.WRKY57 were tested in yeast one‐hybrid assays and showed strong binding activity with conserved sequences containing a W box in the promoters of the B transport‐related genes BnaNIP5;1s and BnaBOR1s. Green fluorescent protein fused to the target protein demonstrated the nuclear localization of BnaA9.WRKY47. CRISPR/Cas9‐mediated knockout lines of BnaA9.WRKY47 in B. napus had increased sensitivity to low B and lower contents of B than wild‐type plants. In contrast, overexpression of BnaA9.WRKY47 enhanced the adaptation to low B with higher B contents in tissues than in wild‐type plants. Consistent with the phenotypic response and B accumulation in these transgenic lines, the transcription activity of BnaA3.NIP5;1, a B efficiency candidate gene, was decreased in the knockout lines but was significantly increased in the overexpressing lines under low B conditions. Electrophoretic mobility shift assays, transient expression experiments in tobacco and in situ hybridizations showed that BnaA9.WRKY47 directly activated BnaA3.NIP5;1 expression through binding to the specific cis‐element. Taken together, our findings support BnaWRKYs as new participants in response to low B, and BnaA9.WRKY47 contributes to the adaptation of B. napus to B deficiency through up‐regulating BnaA3.NIP5;1 expression to facilitate efficient B uptake.

Ovarian ischemia is a gynecological emergency that occurs as a result of ovarian torsion, affects women of reproductive age, and reduces ovarian reserve. The current study was designed to investigate the effect of boric acid taken in different ways on histopathological changes, autophagy, oxidative stress, and DNA damage caused by ischemia and reperfusion in the ovary of adult female rats. We established seven groups of 70 adult female rats: untreated control, intraperitoneal boric acid group (IpBA), oral boric acid group (OBA), ischemia/reperfusion group (ischemia/2 h reperfusion; OIR), ischemia/reperfusion and local boric acid group (OIR + LBA), ischemia/reperfusion and intraperitoneal boric acid group (OIR + IpBA), and ischemia/reperfusion and oral boric acid group (OIR + OBA). On the 31st day of the experimental procedure, both ovaries were harvested for histologic (hematoxylen and eosin and Masson trichrom), biochemical (ELISA and AMH, MDA, SOD, and CAT analyses), and comet evaluation. In the OIR group, hemorrhage, edema, inflammation, and diminished follicle reserve were seen in the ovary. Boric acid treatment reduced the ovarian ischemia/reperfusion damage, and the follicles exhibited similar morphological features to the control group. Moreover, boric acid treatment decreased the levels of Hsp70, NF-KB, COX-2, and CD31, which increased as a result of OIR. On the other hand, SCF and AMH levels, which decreased as a result of OIR, increased with boric acid treatment. The levels of autophagy markers (Beclin-1, LC3, and p62) reached values close to those of the control group. According to the biochemical findings, it was concluded that boric acid is also effective on oxidative stress, and the AMH level was particularly high in the OIR + OBA group, consistent with the immunohistochemical staining result. In addition, it was observed that the DNA damage caused by OIR reached values close to those of the control group, especially in the OBA after OIR. This study showed the therapeutic effects of boric acid on OIR injuries; thus, boric acid may be a potential therapeutic agent for ovarian protection and fertility preservation in cases that may cause ovarian torsion.

Boron (B) is a unique micronutrient for plants given that the range of B concentration from its essentiality to toxicity is extremely narrow, and also because it occurs as an uncharged molecule (boric acid) which can pass lipid bilayers without any degree of controls, as occurs for other ionic nutrients. Boron frequently exceeds the plant’s requirement in arid and semiarid environments due to poor drainage, and in agricultural soils close to coastal areas due to the intrusion of B-rich seawater in fresh aquifer or because of dispersion of seawater aerosol. Global releases of elemental B through weathering, volcanic and geothermal processes are also relevant in enriching B concentration in some areas. Considerable progress has been made in understanding how plants react to B toxicity and relevant efforts have been made to investigate: (I) B uptake and in planta partitioning, (II) physiological, biochemical, and molecular changes induced by B excess, with particular emphasis to the effects on the photosynthetic process, the B-triggered oxidative stress and responses of the antioxidant apparatus to B toxicity, and finally (III) mechanisms of B tolerance. Recent findings addressing the effects of B toxicity are reviewed here, intending to clarify the effect of B excess and to propose new perspectives aimed at driving future researches on the topic.

Limited advancements in managing malignant brain tumors have resulted in poor prognoses for glioblastoma (GBM) patients. Standard treatment involves surgery, radiotherapy, and chemotherapy, which lack specificity and damage healthy brain tissue. Boron-containing compounds, such as boric acid (BA), exhibit diverse biological effects, including anticancer properties. This study aimed to examine whether boron supplementation, as BA, can inhibit glioblastoma growth in a xenograft animal model. Using MRI-based tumor size measurement, survival rates, hematological, clinical biochemistry analyses, and genotoxicity parameters, we assessed the impact of BA. Histopathological, immunohistochemical, and immunofluorescence examinations were also conducted. All BA doses (3.25, 6.5, and 13 mg kg −1 b.w.) extended survival compared to GBM controls after 14 days, with a dose-dependent anti-GBM effect observed in MRI analyses. BA treatment improved hematological (WBC and PLT counts) and biochemical parameters (LDL-C, CREA, and ALP). Histopathological examination revealed a significant reduction in tumor diameter with 6.5 and 13 mg kg −1 BA. Immunohistochemical and immunofluorescence staining showed modulation of intracytoplasmic Ki67, cytoplasmic CMPK2, and GFAP expressions in tumor cells post-BA treatment. Additionally, BA did not increase micronuclei formations, indicating its non-genotoxic nature. In conclusion, targeting tumor suppressor networks with boron demonstrates significant therapeutic potential for GBM treatment.

• Nodulin 26-like intrinsic proteins (NIPs) play essential roles in transporting the nutrients silicon and boron in seed plants, but the evolutionary origin of this transport function and the co-permeability to toxic arsenic remains enigmatic. Horizontal gene transfer of a yet uncharacterised bacterial AqpN-aquaporin group was the starting-point for plant NIP evolution. • We combined intense sequence, phylogenetic and genetic context analyses and a mutational approach with various transport assays in oocytes and plants to resolve the transorganismal and functional evolution of bacterial and algal and terrestrial plant NIPs and to reveal their molecular transport specificity features. • We discovered that aqpN genes are prevalently located in arsenic resistance operons of various prokaryotic phyla. We provided genetic and functional evidence that these proteins contribute to the arsenic detoxification machinery. We identified NIPs with the ancestral bacterial AqpN selectivity filter composition in algae, liverworts, moss, hornworts and ferns and demonstrated that these archetype plant NIPs and their prokaryotic progenitors are almost impermeable to water and silicon but transport arsenic and boron. With a mutational approach, we demonstrated that during evolution, ancestral NIP selectivity shifted to allow subfunctionalisations. • Together, our data provided evidence that evolution converted bacterial arsenic efflux channels into essential seed plant nutrient transporters.