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Aging is closely associated with mitochondrial dysfunction, oxidative stress, and impaired activation of the Nrf2 signaling pathway and all of these contribute to cellular senescence and subsequent cell death. Mitochondrial dysfunction in oxidative stress as well as Mitohormesis on the other hand, remains a paradoxical phenomenon in stress induced ageing and the role of cellular antioxidant like ubiquinol (CoQ10) remains least explored highlighting the need for more research. The present study investigated the cytoprotective properties of ubiquinol in UV-exposed L929 fibroblast cells, emphasizing its dual role in mitigating oxidative damage and enhancing mitochondrial function. Viability results depicted that lower concentrations of ubiquinol (6.25 and 12.5 μg/mL) effectively improved cell viability, reduced ROS levels, and significantly mitigated UV-induced DNA damage, as evidenced by comet assay results. Importantly, ubiquinol treatment enhanced Nrf2 translocation to the nucleus, activating the cell's endogenous antioxidant defense system and promoting cellular resilience attributing to cellular homeostasis. Additionally, ubiquinol mitigated mitochondrial membrane potential (MMP), preventing UV-induced mitochondrial depolarization, a hallmark of dysfunction. This protective effect against mitochondrial damage underscores ubiquinol’s role in maintaining mitochondrial homeostasis in stress induced condition. Moreover, a reduction in senescence-associated β-galactosidase staining was observed, indicating that ubiquinol effectively counteracted cellular senescence. These findings highlight the complex interplay between oxidative stress, mitochondrial function, and Nrf2 activation in aging and Ubiquinol’s ability to mitigate oxidative stress while simultaneously supporting mitochondrial bioenergetics and Nrf2-driven antioxidant responses positions it as a promising cytoprotective compound against UV-induced stress. The experimental results proposes that oxidative homeostasis is revisited in exogenous supplementation of ubiquinol at lower concentrations suggesting that while mild mitochondrial stress may promote longevity, ubiquinol's mitigation of mitochondrial function and oxidative balance could offer a complementary route to achieve cellular wellbeing.
Purpose: To conduct a bibliometric analysis of the Goods and Services Tax (GST) to enhance comprehension of the existing body of knowledge. Design/Methodology/Approach: The analysis was executed using Biblioshiny in R studio, and 784 documents were extracted from the Web of Science (WoS) database covering the years 1989 to 2023. Findings: The analysis findings unveiled prominent authors, highly cited publications, significant themes, keywords, and co-citation networks within the field of GST. Originality/Value: This study used Web of Science (WoS) data for the bibliometric analysis, contributing to the existing literature on this subject. Practical Implications: The research results are pertinent to scholars, researchers, and policymakers in the field of GST. The study offers a roadmap and pathways for scientifically comprehending this domain's current and future research trends.
