Aging is characterized by gradual deterioration of organ or tissue function and its ability to maintain homeostasis of the different physiological processes. This leads to the development of structural and functional alterations accompanied by an increased risk for diverse pathologies. Cellular senescence is a controlled biological process that could contribute to the development of many age-related diseases and related metabolic dysfunctions. Two major chronic diseases associated with premature accumulation of senescent cells that impose an enormous burden on global health systems are obesity and type 2 diabetes mellitus with its related complications. The purpose of this review is to highlight the links between aging, obesity, and type 2 diabetes mellitus, focusing on the role of cellular senescence in disease development and progression. Additionally, this review will discuss the potential of targeting cellular senescence as a promising therapeutic strategy for managing these interrelated diseases, therefore offering a novel approach to prevention and treatment.

• Klíčová slova
• cellular senescence, metabolic complications, obesity, senolytics, type 2 diabetes mellitus,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Chlorinated paraffins (CPs) are environmental pollutants extensively used in industries. While the use of short-chain chlorinated paraffins (SCCPs) has been restricted since 2017, the use of medium-chain chlorinated paraffins (MCCPs) has risen as their replacement. Due to lipophilic character, it can be expected that CPs enter the cells; however, the in vitro accumulation potential of CPs remains poorly understood. In this study, we aimed to explore the ability of SCCPs and MCCPs to accumulate in fat cells. We utilized an in vitro model of mouse 3T3-L1 preadipocytes and adipocytes. Using gas chromatography coupled with high-resolution mass spectrometry operated in negative chemical ionization mode, we determined the intracellular amounts of CPs. These compounds accumulated at rates of 8.5 ± 0.1 µg/gcells/h for SCCPs and 7.8 ± 0.3 µg/gcells/h for MCCPs when an initial concentration of 120 ng/ml was present in the medium. This rate increased approximately tenfold when the concentration of CPs was raised to 1200 ng/ml. CPs content in adipocytes steadily increased over 5 days, whereas preadipocytes accumulated 15-20 times less CPs. This highlights the importance of cellular lipid content, which was about 12 times higher in adipocytes. Furthermore, we found that the level of chlorine content in the CPs molecules significantly influenced their accumulation. Our results demonstrate that MCCPs exhibit a similar accumulation potential to SCCPs, with lipid content playing a crucial role. As with SCCPs, restrictions on the use of MCCPs in industry should be considered to mitigate their environmental and health impacts.

• Klíčová slova
• 3T3-L1 cells, Adipocytes, Chlorinated paraffins, Persistent organic pollutants,
• MeSH
• buňky 3T3-L1 MeSH
• chlorované uhlovodíky * metabolismus   toxicita   MeSH
• halogenace MeSH
• látky znečišťující životní prostředí * metabolismus   toxicita   MeSH
• lipidy analýza   MeSH
• metabolismus lipidů * účinky léků   MeSH
• myši MeSH
• parafín * metabolismus   toxicita   chemie   MeSH
• plynová chromatografie s hmotnostně spektrometrickou detekcí MeSH
• tukové buňky * metabolismus   účinky léků   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• chlorované uhlovodíky * MeSH
• látky znečišťující životní prostředí * MeSH
• lipidy MeSH
• parafín * MeSH