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Autism is a neurodevelopmental disorder distinguished by impaired social interaction and repetitive behaviors. Global estimates indicate that autism affects approximately 1.6% of children, with the condition progressively becoming more prevalent over time. Despite noteworthy progress in autism research, the condition remains untreatable. This serves as a driving force for scientists to explore new approaches to disease management. Autism is linked to elevated levels of oxidative stress and disturbances in the DNA repair mechanism, which may potentially play a role in its comorbidities development. The current investigation aimed to evaluate the beneficial effect of the naturally occurring flavonoid proanthocyanidins on the behavioral characteristics and repair efficacy of autistic BTBR mice. Moreover, the mechanisms responsible for these effects were clarified. The present findings indicate that repeated administration of proanthocyanidins effectively reduces altered behavior in BTBR animals without altering motor function. Proanthocyanidins decreased oxidative DNA strand breaks and accelerated the rate of DNA repair in autistic animals, as evaluated by the modified comet test. In addition, proanthocyanidins reduced the elevated oxidative stress and recovered the disrupted DNA repair mechanism in the autistic animals by decreasing the expressions of and levels and enhancing the expressions of , , and genes. This indicates that proanthocyanidins have significant potential as a new therapeutic strategy for alleviating autistic features.
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http://dx.doi.org/10.1016/j.jsps.2024.102187 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
September 2025
Department of Biology, College of Education for Pure Sciences, University of Kerbala, Kerbala, Iraq.
Gastric cancer is one of the causes of deaths related to cancer across the globe and both genetic and environmental factors are the most prominent. Causes of its pathogenesis. This paper researches the expression of the C-FOS gene.
View Article and Find Full Text PDFBr J Surg
September 2025
Department of Digestive Surgery, CARPEM Comprehensive Cancer Centre, Georges-Pompidou European Hospital, AP-HP, Université Paris-Cité, Paris, France.
Adv Sci (Weinh)
September 2025
School of Stomatology, Xuzhou Medical University, Affiliated Stomatological Hospital of Xuzhou Medical University, Xuzhou, 221004, China.
Musculoskeletal disorders, including bone fractures, osteoarthritis, and muscle injuries, represent a leading cause of global disability, revealing the urgency for advanced therapeutic solutions. However, current therapies face limitations including donor-site morbidity, immune rejection, and inadequate mimicry of dynamic tissue repair processes. DNA-based hydrogels emerge as transformative platforms for musculoskeletal reconstruction, with their sequence programmability, dynamic adaptability, and biocompatibility to balance structural support and biological functions.
View Article and Find Full Text PDFHIV-induced gut microbiota dysbiosis perpetuates mucosal barrier disruption and systemic inflammation despite antiretroviral therapy (ART), creating a tumor-permissive microenvironment. This review synthesizes evidence linking HIV-associated microbial alterations to oncogenesis through three convergent metabolic axes: (1) butyrate deficiency impairing epithelial energy metabolism and anti-tumor immunity; (2) tryptophan metabolism dysregulation compromising gut barrier integrity via depletion and -mediated phenylethylamine overproduction; and (3) vitamin B biosynthesis defects disrupting DNA repair and Th1/Th2 balance. Comparative profiling across HIV-associated malignancies-non-Hodgkin lymphoma, cervical cancer, hepatocellular carcinoma, and lung cancer-reveals conserved dysbiotic signatures: depletion of anti-inflammatory taxa (, ) and expansion of pro-inflammatory genera (, ).
View Article and Find Full Text PDFNAR Cancer
September 2025
Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115, United States.
The mycotoxin, aflatoxin B (AFB), is a potent mutagen that contaminates agricultural food supplies. After ingestion, AFB is oxidized into a reactive electrophile that alkylates DNA, forming bulky lesions such as the genotoxic formamidopyrimidine lesion, AFB-Fapy dG. This lesion is mainly repaired by nucleotide excision repair (NER) in bacteria; however, in humans the picture is less clear.
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