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Lymphotoxin-beta (LT-beta) (Tumor necrosis factor C) (TNF-C) (Tumor necrosis factor ligand superfamily member 3) [TNFC] [TNFSF3]


Aging and Hyperglycemia Intensify Dyslipidemia-Induced Oxidative Stress and Inflammation in Rats: Assessment of Restorative Potentials of ALA and EPA DHA.

Effect of aging and hyperglycemia on oxidative stress (OS) and inflammation in dyslipidemic conditions has not been elucidated. Hence, in this study, we assessed the implications of aging, hyperglycemia, and also the dietary effect of n-3 fatty acids (α-linolenic acid (ALA) and eicosapentaenoic acid (EPA) docosahexaenoic acid (DHA)) on OS and inflammation in dyslipidemic rats. Dyslipidemia was induced in young and aged rats by feeding high-fat lard (HFL) diet. Diabetes was induced in young dyslipidemic rats by administering streptozotocin 30 days after the induction of dyslipidemia. Experimental groups received diets containing canola oil (HF CNO) and fish oil (HF FO) as a source of ALA and EPA DHA respectively. After 60 days of feeding rats with their respective diets, OS and inflammatory markers in serum were assessed. Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE , LTB , and LTC ) level in serum of both young and aged rats. Aged dyslipidemic rats presented significantly (p < 0.05) higher level of these markers compared to young dyslipidemic rats. Hyperglycemia onset further augmented OS and inflammatory markers in young dyslipidemic rats significantly (p < 0.05). Administration of n-3 fatty acids downregulated the serum markers of OS and inflammation in all the three experimental models. Thus, aging and hyperglycemia onset intensified dyslipidemia-induced OS and inflammation. Dietary preformed EPA DHA presented larger restorative potentials than precursor ALA in countering OS and inflammation in all the three experimental models.

MeSH Terms

  • Aging
  • Animals
  • Biomarkers
  • Diabetes Mellitus, Experimental
  • Docosahexaenoic Acids
  • Dyslipidemias
  • Eicosapentaenoic Acid
  • Fatty Acids, Omega-3
  • Hyperglycemia
  • Inflammation
  • Oxidative Stress
  • Rats
  • alpha-Linolenic Acid


  • dyslipidemia
  • hyperglycemia
  • inflammation
  • n-3 fatty acids
  • oxidative stress

Advanced age in mares affects endometrial secretion of arachidonic acid metabolites during equine subclinical endometritis.

Even if mares continue to breed up to an advanced age, in aging mares reproductive failure is quite common. Subclinical endometritis, which occurs more often in aging mares than in younger counterparts, may cause prolongation or shortening of the inter-estrus period or the corpus luteum lifespan. We hypothesized that during subclinical endometritis the secretion of selected arachidonic acid metabolites may differ in aging mares compared to younger females. To verify this thesis, ex vivo organ cultures of endometrium were established with subsequent measurements of concentrations of prostaglandin E (PGE ), 6-keto-PGF and both leukotrienes (LTs), LTB and LTC in the culture supernatants. The endometrial biopsies were obtained from 82 mares of known breeding history. This study revealed that the concentrations of the selected arachidonic acid metabolites, which act both as immunological mediators and endocrine modulators in the reproductive organs, depends on the mares' ages. Spontaneous endometrial secretion of PGE , 6-keto-PGF and LTC was increased in mares aged 16-23 years that suffered from subclinical endometritis, compared with control counterparts. Moreover, secretion of these metabolites was higher in endometritis-positive mares aged 16-23 years than in younger females. We conclude that advanced age in mares further disturbs the immuno-endocrine balance in endometritis-positive mares.

MeSH Terms

  • Aging
  • Animals
  • Arachidonic Acid
  • Endometritis
  • Female
  • Horse Diseases
  • Horses


  • Aging
  • Arachidonic acid metabolites
  • Mare
  • Subclinical endometritis