BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091264
Olga Riusech, Lingjun Li
{"title":"Isotopic <i>N</i>,<i>N</i>-Dimethyl Leucine-Based Mass Spectrometric Quantification of Metabolites Following Copper Exposure.","authors":"Olga Riusech, Lingjun Li","doi":"10.3390/biom15091264","DOIUrl":"10.3390/biom15091264","url":null,"abstract":"<p><p>Crustaceans are particularly sensitive to copper toxicity, and although the downstream effects of increased copper exposure on the metabolome are often postulated and observed, they are rarely measured. To perform absolute quantification of hydrophilic small-molecule metabolites in the hemolymph of the crustacean <i>Cancer borealis</i>, we derivatized targeted metabolites related to copper toxicity using in-house-developed isotopic <i>N</i>,<i>N</i>-dimethyl leucine (iDiLeu) tags. Selected analytes were pooled at previously determined concentrations to serve as internal standards, and a calibration curve was generated. The sample loss was minimized by optimizing the derivatization-assisted sample cleanup using dispersive liquid-liquid microextraction (DLLME) and hydrophilic-lipophilic balancing (HLB). Calibration curves were then used for the absolute quantification of metabolites of interest following 30 min, 1 h, and 2 h exposures to 10 µM CuCl<sub>2</sub>. We found that glutamic acid was downregulated after 2 h of copper exposure, which may disrupt cellular metabolism and increase oxidative stress in crustaceans. These changes could have significant impacts on crustacean populations and the ecosystems they support.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091265
Spyridon Marios Giatro, George Komontachakis, Aikaterini Kalantidou, Nastazia Lesgidou, Vlasios Karageorgos, Mohamed Teleb, Md Rabiul Islam, Thomas Mavromoustakos, Hesham Fahmy, Maria Venihaki, Minos-Timotheos Matsoukas, George Liapakis
{"title":"Pharmacological Characterization of the Novel CRF1 Receptor Antagonist, Thiazolo[4,5-d] Pyrimidine Analog, M43.","authors":"Spyridon Marios Giatro, George Komontachakis, Aikaterini Kalantidou, Nastazia Lesgidou, Vlasios Karageorgos, Mohamed Teleb, Md Rabiul Islam, Thomas Mavromoustakos, Hesham Fahmy, Maria Venihaki, Minos-Timotheos Matsoukas, George Liapakis","doi":"10.3390/biom15091265","DOIUrl":"10.3390/biom15091265","url":null,"abstract":"<p><p>The corticotropin-releasing factor (CRF) and its type 1 receptor (CRF<sub>1</sub>R) play a key role in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Dysregulation of the HPA axis is associated with congenital adrenal hyperplasia (CAH) and depression. Non-peptide CRF<sub>1</sub>R-selective antagonists displayed antidepressant effects on animal models and are used for the management of CAH. To develop novel non-peptide CRF<sub>1</sub>R antagonists, we have previously designed and synthesized a series of substituted pyrimidines. Among these analogs, molecule 43 (M43) binds to CRF<sub>1</sub>R with the highest affinity. Based on this finding, we selected M43 for further pharmacological characterization in the present study. The results suggest that M43 is a potent CRF<sub>1</sub>R antagonist, blocking the ability of the CRF-related agonist, Tyr<sup>0</sup>-sauvagine, to stimulate (1) cAMP accumulation in HEK 293 cells expressing CRF<sub>1</sub>R and (2) the proliferation rate of RAW 264.7 macrophages. Computational studies suggest that the antagonist properties of M43 are mostly attributed to its ability to interact with residues in the allosteric pocket of CRF<sub>1</sub>R, comprised of the third, fifth, and sixth transmembrane domain residues, which block activation-associated structural rearrangements of the receptor. Our data will be used to design novel non-peptide CRF<sub>1</sub>R antagonists for clinical use.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091267
Slàine F Chaimbeul, Nubia N P Rodrigues, Danny D Thurston, Kirsten E Scoggin, Jennifer Janes, Cale A Jacobs, James N MacLeod, Austin V Stone, Bruno C Menarim
{"title":"PPARγ Agonism Modulates Synovial Macrophage and Cartilage Responses in an Equine Model of Synovial Inflammation-Implications for Joint Therapy.","authors":"Slàine F Chaimbeul, Nubia N P Rodrigues, Danny D Thurston, Kirsten E Scoggin, Jennifer Janes, Cale A Jacobs, James N MacLeod, Austin V Stone, Bruno C Menarim","doi":"10.3390/biom15091267","DOIUrl":"10.3390/biom15091267","url":null,"abstract":"<p><p>Synovitis resolution is critical for joint homeostasis and prevents the progression of osteoarthritis (OA). Treatments like NSAIDs and intra-articular corticosteroids relieve symptoms by blocking pro-inflammatory mediators, but also impair the production of pro-resolving mediators, contributing to the likelihood of chronic synovitis. PPARγ signaling is an essential mechanism of synovitis resolution, which is decreased in OA tissues. To evaluate the potential of PPARγ agonists to promote pro-resolving pathways, equine macrophages cultured in autologous, normal, or inflamed synovial fluid (<i>n</i> = 10 horses) were treated with pioglitazone, geraniol, or both. Treatments modulated patterns of gene expression, increasing the expression of early drivers of resolution <i>RELB</i> and <i>IL6</i>, followed by increased <i>NRF2</i> and <i>PPARGC1A</i> expression. Concentrations of TNF-α in conditioned synovial fluid significantly decreased as an early response to treatment, while IL10 concentrations also declined over time, suggesting increased tolerance to inflammatory stimuli and decreased compensatory feedback. Using an equine model of synovitis, intra-articular delivery of pioglitazone (<i>n</i> = 3 horses) or geraniol (<i>n</i> = 4 horses) was associated with decreased markers of synovium inflammation (geraniol) and enhanced cartilage proteoglycan preservation (geraniol and pioglitazone). In this small cohort of horses, no systemic or articular side effects were observed. Further studies optimizing treatment doses and regimens for intra-articular PPARγ agonism as a pro-resolving OA therapy are warranted.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091266
Subrata H Mishra, Sujan Chatterjee, Loretta Viera-Preval, Prasun Guha
{"title":"From Obscurity to Prominence: IPMK's Expanding Role in Cellular Signaling, Physiology, and Disease.","authors":"Subrata H Mishra, Sujan Chatterjee, Loretta Viera-Preval, Prasun Guha","doi":"10.3390/biom15091266","DOIUrl":"10.3390/biom15091266","url":null,"abstract":"<p><p>Once a protein of relative obscurity, inositol polyphosphate multikinase (IPMK) emerged as a versatile and indispensable enzyme in cellular biology. With dual inositol and lipid kinase activities, IPMK generates pivotal signaling molecules such as InsP4 (inositol tetraphosphate), InsP5 (inositol pentaphosphate), and PIP3 (phosphoinositide 3,4,5-trisphosphate), positioning it as a critical regulator of cellular mechanisms. Initially identified in yeast and later recognized as essential for mammalian embryonic development, IPMK has transitioned from a niche interest to a focal point in studies of nutrient sensing, growth factor signaling, mRNA transport, and transcription regulation. Over two decades, multidisciplinary research has unveiled its far-reaching biological roles and implications in diverse diseases, including neurodegeneration, cancer, and inflammation. This review charts IPMK's journey from obscurity to prominence, examining its structure-function relationships, cellular roles, and emerging physiological impacts, while highlighting its potential as a therapeutic target in human health and disease.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091268
Rosanna Squitti, Alberto Benussi, Silvia Fostinelli, Andrea Geviti, Jasmine Rivolta, Mariacarla Ventriglia, Alessandra Micera, Mauro Rongioletti, Roberta Ghidoni, Matteo Santilli, Alberto Granzotto, Alberto Albanese, Giuliano Binetti, Stefano L Sensi, Barbara Borroni
{"title":"Zinc Therapy in Mild Cognitive Impairment: Cognitive Stabilization in Pharmacodynamically Responsive Patients in the ZINCAiD Trial.","authors":"Rosanna Squitti, Alberto Benussi, Silvia Fostinelli, Andrea Geviti, Jasmine Rivolta, Mariacarla Ventriglia, Alessandra Micera, Mauro Rongioletti, Roberta Ghidoni, Matteo Santilli, Alberto Granzotto, Alberto Albanese, Giuliano Binetti, Stefano L Sensi, Barbara Borroni","doi":"10.3390/biom15091268","DOIUrl":"10.3390/biom15091268","url":null,"abstract":"<p><p>Dysregulation contributes to Alzheimer's disease (AD) pathophysiology. Zinc therapy promotes enterocyte copper sequestration, potentially reducing systemic copper. Individual biological responses may vary.</p><p><strong>Methods: </strong>ZINCAiD was a 24-week, randomized, double-blind, placebo-controlled phase II trial assessing zinc therapy in individuals with mild cognitive impairment (MCI) due to AD (EudraCT No.: 2019-000604-15; registered on 26 March 2020). Participants were randomized 2:1 to receive elemental zinc (135 mg/day for 12 weeks, then 65 mg/day) or placebo. Ceruloplasmin was measured at predefined intervals for safety monitoring, blinded to the investigators. Post hoc, \"Zinc Responders\" were defined by ≥20% reduction in ceruloplasmin at week 12. The primary cognitive endpoint was the Cognitive Composite 2 scale (CC2); secondary endpoints included MMSE and CDR-Sob.</p><p><strong>Findings: </strong>Of the 48 participants randomized, 9 discontinued, primarily due to unrelated clinical deterioration; 39 had complete ceruloplasmin data. Two serious adverse events occurred in the Placebo group. Mild gastrointestinal symptoms occurred in eight participants, with only four leading to dropout. In the primary zinc vs. placebo analysis, no significant differences emerged in cognitive outcomes. A post hoc exploratory analysis stratified participants by pharmacodynamic response: 12 individuals with MCI due to AD (31%) met the criteria for \"Zinc Responder,\" defined by ≥20% reduction in serum ceruloplasmin at week 12. Only Zinc Responders maintained cognitive stability over 24 weeks, whereas the combined group of Zinc Non-Responders and placebo-treated participants showed a significant decline. For the composite cognitive score (CC2), the interaction between visit and response group was significant (<i>p</i> = 0.030), with deterioration observed only in the Non-Responder + Placebo group (Δ = -2.72, <i>p</i> < 0.0001 vs. -0.71, <i>p</i> = 0.35 in Responders). Similar patterns were observed for CDR-Sob (interaction <i>p</i> = 0.017) and MMSE (trend <i>p</i> = 0.09).</p><p><strong>Interpretation: </strong>Zinc therapy stabilized cognition in a pharmacodynamically defined MCI subgroup. These exploratory findings suggest serum ceruloplasmin as a feasible biomarker of target engagement. Larger trials are needed for confirmation.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091262
João Moura, Pietro Antenucci, Ester Coutinho, Kailash P Bhatia, Lorenzo Rocchi, Anna Latorre
{"title":"Neuromyotonia and CASPR2 Antibodies: Electrophysiological Clues to Disease Pathophysiology.","authors":"João Moura, Pietro Antenucci, Ester Coutinho, Kailash P Bhatia, Lorenzo Rocchi, Anna Latorre","doi":"10.3390/biom15091262","DOIUrl":"10.3390/biom15091262","url":null,"abstract":"<p><p>Contactin-associated protein-like 2 (CASPR2) is a transmembrane protein of the neurexin superfamily, essential for clustering voltage-gated potassium channels, particularly Kv1, at the juxtaparanodal regions of myelinated axons. This precise localisation is essential for maintaining normal axonal excitability and preventing aberrant signal propagation. Autoantibodies targeting CASPR2 have been associated with various neurological syndromes, notably peripheral nerve hyperexcitability (PNH), which presents clinically with neuromyotonia and myokymia. PNH is characterised by distinctive electrophysiological findings, including neuromyotonic discharges, myokymic discharges, and afterdischarges, which provide diagnostic value and insight into underlying pathophysiology. This review explores the mechanisms of anti-CASPR2-associated PNH, focusing on how antibody-mediated disruption of Kv1 channel clustering leads to altered axonal excitability. Current evidence suggests that both the distal and proximal segments of the axon are sites of pathological activity, where impairments in action potential termination and re-entry prevention result in spontaneous, repetitive discharges. While afterdischarges likely originate within the axon, the precise location-whether in the alpha-motoneuron soma or axon-is uncertain. The involvement of spinal inhibitory circuits has also been proposed, though it remains speculative. Understanding the neurophysiological features of anti-CASPR2-associated PNH is essential for improving diagnostic accuracy and guiding treatment strategies. Further research is needed to clarify the mechanisms of CASPR2-related hyperexcitability.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-09-01DOI: 10.3390/biom15091263
Yan Ma, Jun Zhang, Yaxuan Qi, Yating Lu, Yalan Dong, Desheng Hu
{"title":"Neutrophil Extracellular Traps in Cardiovascular Diseases: Pathological Roles and Therapeutic Implications.","authors":"Yan Ma, Jun Zhang, Yaxuan Qi, Yating Lu, Yalan Dong, Desheng Hu","doi":"10.3390/biom15091263","DOIUrl":"10.3390/biom15091263","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) is currently recognized as one of the leading health threats to humanity. Neutrophils play an important role in innate immune response. The activation of neutrophils leads to the release of neutrophil extracellular traps (NETs) in response to various stimuli. Appropriate NETs are essential for maintaining homeostasis in the body, while excessive NETs will cause pathological damage. Accumulating evidence indicates that NETs are implicated in CVD pathophysiology. This review aims to provide a comprehensive review of the characteristics, signaling pathways, and interactions of NETs with other immune cells, and the comparisons of NETosis with other cell deaths, focusing on the role of NETs in CVDs. Furthermore, this study provides a theoretical basis for further improvement in targeted NET therapy for CVD.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-08-30DOI: 10.3390/biom15091259
Drucy Borowitz
{"title":"Non-Pancreatic Digestive Enzymes.","authors":"Drucy Borowitz","doi":"10.3390/biom15091259","DOIUrl":"10.3390/biom15091259","url":null,"abstract":"<p><p>Although the pancreas is the organ that produces the most critical digestive enzymes, there are other important contributors to the cleavage of food into absorbable units. Pre-pancreatic digestion of carbohydrates occurs through the action of salivary amylase. Pre-pancreatic digestion of fats is mediated by lingual and gastric lipases, and their action may be important as a signal for coordinated digestion. Pepsin, which is present in the stomach, initiates the digestion of dietary proteins into peptides and amplifies distal proteolysis. The major post-pancreatic intestinal carbohydrate-digesting enzymes are sucrase-isomaltase, maltase-glucoamylase and lactase-phlorizin hydrolase. There are no post-pancreatic mucosal enzymes that act on dietary triglycerides; however, the complete digestion of phospholipids depends on several brush border phospholipases. Intestinal processing is an important contributor to digestion of proteins, although mucosal proteases may serve as signaling proteins rather than as primary adjuncts to dietary protein digestion and absorption. This review describes the role of these non-pancreatic digestive enzymes in supporting nutritional health.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-08-30DOI: 10.3390/biom15091258
Alessandra Chiarot, Mahek Minhas, Nicoletta M de Maat, Jenny Doan, Mats I Nilsson, Bart P Hettinga, Mehrnoosh Faghih, Michael S Neal, Joshua P Nederveen, Mark A Tarnopolsky
{"title":"A Multi-Ingredient Supplement Improves Body Re-Composition, Ovarian Aging Markers, and Reproductive Success in Young and Middle-Aged Female Mice.","authors":"Alessandra Chiarot, Mahek Minhas, Nicoletta M de Maat, Jenny Doan, Mats I Nilsson, Bart P Hettinga, Mehrnoosh Faghih, Michael S Neal, Joshua P Nederveen, Mark A Tarnopolsky","doi":"10.3390/biom15091258","DOIUrl":"10.3390/biom15091258","url":null,"abstract":"<p><p>Ovarian aging is characterized by mitochondrial dysfunction, oxidative stress, and inflammation. The development of adjunctive treatments that mitigate age-related subfertility is warranted. We examined the benefits of nutraceutical supplementation (FE; Fertility Enhancer) with mitochondrial antioxidants, anti-inflammatory agents, metabolic activators, vitamins and minerals, and amino acids on ovarian aging, metabolic activity, and reproductive success in young (Y; 6-month-old) and middle-aged (O; 11-month-old) female C57BL/6J mice. The mice were fed calorie- and macronutrient-matched diets w/wo the FE supplement for three months and harem mated twice. Daily FE supplementation promoted significant body re-composition, including loss of white adipose tissue (gWAT: -36% vs. CON, <i>p</i> < 0.001), gain of skeletal muscle (SkM: +67% vs. CON, <i>p</i> < 0.001), and improved SkM/gWAT ratio (+185% vs. CON, <i>p</i> < 0.001). Metabolic testing showed enhanced fat oxidation (+38%, <i>p</i> < 0.01) and energy expenditure (+7%, <i>p</i> = 0.051) in FE mice. Breeding and immunoblotting data demonstrated improved reproductive success (Y-CON: 44%, Y-FE: 89%, O-CON: 0%, O-FE: 18%) and a modest attenuation of ovarian aging markers in both FE groups. We surmise that a multi-ingredient supplement, such as the Fertility Enhancer, may improve body re-composition, metabolic activity, and markers of ovarian aging, thus enhancing reproductive health and fertility in females.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiomoleculesPub Date : 2025-08-30DOI: 10.3390/biom15091257
Melissa Parent, Christine Bone, Lee-Anne Huber, E James Squires
{"title":"In Vitro and In Vivo Comparisons of Activated Charcoal and Biochar as Dietary Treatments for Controlling Boar Taint.","authors":"Melissa Parent, Christine Bone, Lee-Anne Huber, E James Squires","doi":"10.3390/biom15091257","DOIUrl":"10.3390/biom15091257","url":null,"abstract":"<p><p>Activated charcoal (AC) is an adsorbent that can prevent the accumulation of boar taint-causing compounds in the fat, but is not an approved dietary additive for livestock animals. Biochar (BC) is a similar feed-approved charcoal adsorbent that may be an alternative dietary additive to control boar taint. This study was conducted to evaluate AC and BC, both in vitro and in vivo, as dietary treatments for boar taint. This was done by first conducting an in vitro binding study to compare binding between AC, BC, and spent filter aid (SFA) for boar taint compounds. Results of the in vitro study showed that both AC and BC had significantly higher <i>B<sub>max</sub></i> for androstenone (AC: 97.2 ± 0.4% and BC: 84.5 ± 0.8%) and skatole (AC: 106.1 ± 0.2%, BC: 113.2 ± 0.7%), compared to SFA with a <i>B<sub>max</sub></i> of 50.5 ± 0.2% for androstenone and 97.1 ± 5.3% for skatole. AC and BC were then tested as feed additives in finisher diets fed to slaughter weight boars. Both adsorbents were successful at preventing boar taint in a subset of animals (83%), while having no effect on plasma levels of estrone sulfate or androstenone, and growth and performance parameters. These findings suggest that BC is a suitable alternative for AC as a dietary additive to prevent boar taint.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}