RESUMEN
One of the key factors influencing aging and morbidity is the overall antioxidant status and regenerative capacity. In examining contributors to the antioxidant status, we analyzed the thiamine status in felines and the influence of age, gender, and body condition score. We measured erythrocytic B1-dependent specific transketolase (STKT) activity, an enzyme in the pentose phosphate pathway, in a group of 60 sexually intact, healthy, and specific pathogen-free felines (44 females, 16 males, aged 1-17 years) with thiamine diphosphate (TDP; 0.3 and 3 mM) and without it. Only two parameters (STKT activity with and without 0.3 mM TDP) decreased with age. After adjusting for age, statistical thresholds were established using these and other age-independent parameters, identifying 15 felines with subclinical thiamine deficiency. The red blood cell proteomics analysis revealed that the pentose phosphate shunt, glycolysis, and oxidative stress response were the most affected pathways in deficient felines, confirming the above diagnosis. Age emerged as the primary factor associated with thiamine deficiency, supported by the enrichment of neurodegenerative diseases with a proteotoxicity component; five young-adult felines showed marginal or acute B1 deficiency, and six were adult-mature with a more chronic deficiency, possibly linked to cognitive decline, all with an underweight to ideal body condition scores. Only three senior-adult felines were deficient and overweight-obese. Detecting thiamine deficiency emphasizes the need for more accurate reference values, the establishment of advanced preventive or therapeutic measures to enhance the well-being of aging companion animals, and potential extensions to human health, particularly concerning cognitive function.
RESUMEN
Changes in mitochondrial dynamics are often associated with dietary patterns, medical treatments, xenobiotics, and diseases. Toxic exposures to hydrogen sulfide (H2S) harm mitochondria by inhibiting Complex IV and via other mechanisms. However, changes in mitochondrial dynamics, including morphology following acute exposure to H2S, are not yet fully understood. This study followed mitochondrial morphology changes over time after a single acute LCt50 dose of H2S by examining electron microscopy thalami images of surviving mice. Our findings revealed that within the initial 48 h after H2S exposure, mitochondrial morphology was impaired by H2S, supported by the disruption and scarcity of the cristae, which are required to enhance the surface area for ATP production. At the 72-h mark point, a spectrum of morphological cellular changes was observed, and the disordered mitochondrial network, accompanied by the probable disruption of mitophagy, was tied to changes in mitochondrial shape. In summary, this study sheds light on how acute exposure to high levels of H2S triggers alterations in mitochondrial shape and structure as early as 24 h that become more evident at 72 h post-exposure. These findings underscore the impact of H2S on mitochondrial function and overall cellular health.
