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Vazquez-Medina, J. P.

Publications and source records attributed to Vazquez-Medina, J. P..

4 recordsLinked to original sources

Oxidative stress is a potential cost of synchronous nesting in olive ridley sea turtles

Olive ridley sea turtles, Lepidochelys olivacea, exhibit a polymorphic reproductive behaviour nesting in solitary or in mass aggregations termed "arribadas", where thousands of turtles nest at once. Arribadas may provide fitness benefits including mate finding during nearshore aggregations and predator satiation at the time of hatching, but the potential costs of arribada nesting remain understudied. To explore the potential trade-offs of the fitness benefits associated with arribada nesting, we collected blood from olive ridley turtles nesting in arribada and solitary. We measured reproductive and metabolic hormones (progesterone, estradiol, testosterone, thyroxine, and triiodothyronine), triglycerides (TG), non-esterified fatty acids (NEFA) and markers of oxidative damage (4-hydroxynonenal, malondialdehyde, protein carbonyls, and nitrotyrosine). Arribada nesters were bigger and had higher levels of progesterone than solitary nesters. Similarly, thyroid hormones were higher in individuals nesting in arribada than in solitary nesters, while TG and NEFA were positively correlated in arribada but not in solitary nesters. Nesting in arribada was associated with increased lipid peroxidation and protein carbonyls compared to solitary nesting. These results suggest that nesting in arribada is potentially more energetically expensive than nesting solitarily, and that oxidative stress may be a trade-off of the fitness benefits associated with arribada nesting.

physiology

Short-term elevations in glucocorticoids do not alter telomere lengths: A systematic review and meta-analysis of non-primate vertebrate studies

BackgroundThe neuroendocrine stress response allows vertebrates to cope with stressors via the activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis, which ultimately results in the secretion of glucocorticoids (CORT). Glucocorticoids have pleiotropic effects on behavior and physiology, and might influence telomere length dynamics. During a stress event, CORT mobilizes energy towards survival mechanisms rather than to telomere maintenance. Additionally, reactive oxidative species produced in response to increased CORT levels can damage telomeres, also leading to telomere shortening. In our systematic review and meta-analysis, we tested whether CORT levels impact telomere length and if this relationship differs among time frame, life history stage, or stressor type. We hypothesized that elevated CORT levels are linked to a decrease in telomere length. MethodsTo test this hypothesis, we conducted a literature search for studies investigating the relationship between telomere length and CORT levels in non-human vertebrates using four search engines: Web of Science, Google Scholar, Pubmed and Scopus, last searched on September 27th, 2020. This review identified 31 studies examining the relationship between CORT and telomere length. We pooled the data using Fishers Z for 15 of these studies. All quantitative studies underwent a risk of bias assessment. This systematic review study was registered in the Open Science Framework Registry (https://osf.io/rqve6). ResultsThe pooled effect size from fifteen studies and 1066 study organisms shows no relationship between CORT and telomere length ((Fishers Z= 0.1042, 95% CI = 0.0235; 0.1836). While these results support some previous findings, other studies have found a direct relationship between CORT and telomere dynamics, suggesting underlying mechanisms or concepts that are not currently taken into account in our analysis. The risk of bias assessment revealed an overall low risk of bias with occasional instances of bias from missing outcome data or bias in the reported result. ConclusionWe highlight the need for more targeted experiments to understand how conditions, such as experimental timeframes, stressor(s), and stressor magnitudes can drive a relationship between the neuroendocrine stress response and telomere length.

physiology

Repeated stimulation of the HPA axis alters white blood cell counts without increasing oxidative stress or inflammatory cytokines in fasting elephant seal pups

The hypothalamic-pituitary-adrenal (HPA) axis controls the release of glucocorticoids, which regulate immune and inflammatory function by modulating cytokines, white blood cells (WBCs), and oxidative stress via glucocorticoid receptor (GR) signaling. Although the response to HPA activation is well characterized in many species, little is known about the impacts of HPA activation during extreme physiological conditions in marine mammals. Hence, we challenged 18 simultaneously fasting and developing elephant seal pups with daily intramuscular injections of adrenocorticotropin (ACTH), a GR antagonist (RU486), or a combination (ACTH+RU486) for four days (4d). We collected blood at baseline, two hours (2h), and 4d after the beginning of treatment. ACTH and ACTH+RU486 elevated serum aldosterone and cortisol at 2h, with effects diminishing at 4d. RU486 alone induced a compensatory increase in aldosterone, but not cortisol, at 4d. ACTH decreased neutrophils at 2h while decreasing lymphocytes and increasing neutrophil:lymphocyte ratio at 4d. These effects were abolished by RU486. Despite alterations in WBCs, there was no effect of ACTH or RU486 on transforming growth factor-{beta} or interleukin-6 levels; however, both cytokines decreased with the 4-d fasting progression. Similarly, ACTH did not impact protein oxidation, lipid peroxidation, or antioxidant enzymes, but plasma isoprostanes and catalase activity decreased while glutathione peroxidase increased with fasting progression. These data demonstrate differential acute (2h) and chronic (4d) modulatory effects of HPA activation on WBCs and that the chronic effect is mediated, at least in part, by GR. These results also underscore elephant seals resistance to potential oxidative stress derived from repeated HPA activation. Summary statementMany species experience oxidative stress and inflammation after repeated activation of the hypothalamic-pituitary-adrenal axis. We show that simultaneously fasting and developing elephant seals are resistant to repeated hypothalamic-pituitary-adrenal axis activation.

physiology

Elephant seal muscle cells adapt to sustained glucocorticoid exposure by shifting their metabolic phenotype

Elephant seals experience natural periods of prolonged food deprivation while breeding, molting, and undergoing postnatal development. Prolonged food deprivation in elephant seals increases circulating glucocorticoids without inducing muscle atrophy, but the cellular mechanisms that allow elephant seals to cope with such conditions remain elusive. We generated a cellular model and conducted transcriptomic, metabolic, and morphological analyses to study how seal cells adapt to sustained glucocorticoid exposure. Seal muscle progenitor cells differentiate into contractile myotubes with a distinctive morphology, gene expression profile, and metabolic phenotype. Exposure to dexamethasone at three ascending concentrations for 48h modulated the expression of 6 clusters of genes related to structural constituents of muscle and pathways associated with energy metabolism and cell survival. Knockdown of the glucocorticoid receptor (GR) and downstream expression analyses corroborated that GR mediates the observed effects. Dexamethasone also decreased cellular respiration, shifted the metabolic phenotype towards glycolysis, and induced mitochondrial fission and dissociation of mitochondria-ER interactions without decreasing cell viability. Knockdown of DDIT4, a GR target involved in the dissociation of mitochondria-ER membranes, recovered respiration and modulated antioxidant gene expression. These results show that adaptation to sustained glucocorticoid exposure in elephant seal myotubes involves a metabolic shift toward glycolysis, which is supported by alterations in mitochondrial morphology and a reduction in mitochondria-ER interactions, resulting in decreased respiration without compromising cell survival.

physiology