Oxidative stress and food supplementation with antioxidants in therapy dogs.

The objective of this study was to evaluate the ability of a long-term antioxidant-supplemented diet to regulate the oxidative stress and general health status of dogs involved in animal-assisted intervention (AAI) programs. Oxidative stress is a consequence of the accumulation of reactive oxygen species (ROS). Exercise-induced oxidative stress can increase muscle fatigue and fiber damage and eventually leads to impairment of the immune system. A randomized, placebo-controlled, crossover clinical evaluation was conducted with 11 healthy therapy dogs: 6 females and 5 males of different breeds and with a mean age of 2.7 ± 0.8 y (mean ± SEM). The dogs were divided into 2 groups, 1 fed a high quality commercial diet without antioxidants (CD) and the other a high quality commercial diet supplemented with antioxidants (SD) for 18 wk. After the first 18 wk, metabolic parameters, reactive oxygen metabolite-derivatives (d-ROMs), and biological antioxidant potential (BAP) levels were monitored and showed a significant reduction of d-ROMs, triglycerides, and creatinine values in the SD group (P < 0.05) and a significant increase in amylase values in the CD group (P < 0.01). At the end of this period, groups were crossed over and fed for another 18 wk. A significant decrease in amylase and glutamate pyruvate transaminase (GPT) values was observed in the CD and SD group, respectively (P < 0.05). In conclusion, a controlled, balanced antioxidant diet may be a valid approach to restoring good cell metabolism and neutralizing excess free radicals in therapy dogs.

L'objectif de la présente étude était d'évaluer la capacité d'une diète long-terme supplémentée en antioxydant à réguler le stress oxydatif et l'état de santé général de chiens impliqués dans des programmes d'intervention avec assistance animale (IAA). Le stress oxydatif est une conséquence de l'accumulation d'espèces oxygène réactive (EOR). Le stress oxydatif induit par l'exercice peut augmenter la fatigue musculaire et les dommages aux fibres et éventuellement mener à un mauvais fonctionnement du système immunitaire. Une évaluation clinique croisée, randomisée, et avec groupe témoin-placebo a été menée avec 11 chiens d'assistance en santé : 6 femelles et 5 mâles de races différentes et d'un âge moyen de 2,7 ± 0,8 ans (moyenne ± écart-type). Les chiens ont été divisés en deux groupes, un premier groupe nourri avec une diète commerciale de haute qualité sans antioxydant (DC) et l'autre groupe avec une diète commerciale de haute qualité supplémentée avec des antioxydants (DS) pour 18 semaines. Après les premières 18 semaines, les paramètres métaboliques, les métabolites dérivés d'oxygène réactive (MDOR), et les niveaux de potentiel antioxydant biologique (PAB) ont été surveillés et ont montré une réduction significative des valeurs des MDOR, des triglycérides et de la créatinine dans le groupe DS (P < 0,05) et une augmentation significative des valeurs de l'amylase dans le groupe DC (P < 0,01). À la fin de cette période, les groupes ont été croisés et nourris pour 18 semaines supplémentaires. Une diminution significative des valeurs de l'amylase et de la glutamate pyruvate transaminase (GPT) a été obtenue dans les groupes DC et DS, respectivement (P < 0,05). En conclusion, une diète contrôlée, balancée en antioxydant pourrait être une approche valide pour restaurer un bon métabolisme cellulaire et neutraliser les radicaux libres excédentaires chez les chiens d'assistance.(Traduit par Docteur Serge Messier).

An Antioxidant Dietary Supplement Improves Brain-Derived Neurotrophic Factor Levels in Serum of Aged Dogs: Preliminary Results.

Biological aging is characterized by a progressive accumulation of oxidative damage and decreased endogenous antioxidant defense mechanisms. The production of oxidants by normal metabolism damages proteins, lipids, and nucleotides, which may contribute to cognitive impairment. In this study 36 dogs were randomly divided into four groups and fed croquettes of different compositions for 6 months. We monitored derivatives of reactive oxygen metabolites (dROMs) and biological antioxidant potential (BAP) levels in dogs' plasma samples as well as brain-derived neurotrophic factor (BDNF) serum levels at the beginning and at the end of the dietary regime. Our results showed that a dietary regime, enriched with antioxidants, induced a significant decrease of plasma levels of dROMs (p < 0.005) and a significant increase in BDNF serum levels (p < 0.005) after six months. Thus, we hypothesized a possible role of the diet in modulating pro- and antioxidant species as well as BDNF levels in plasma and serum, respectively. In conclusion the proposed diet enriched with antioxidants might be considered a valid alternative and a valuable strategy to counteract aging-related cognitive decline in elderly dogs.

NUP98 fusion oncoproteins promote aneuploidy by attenuating the mitotic spindle checkpoint.

NUP98 is a recurrent fusion partner in chromosome translocations that cause acute myelogenous leukemia. NUP98, a nucleoporin, and its interaction partner Rae1, have been implicated in the control of chromosome segregation, but their mechanistic contributions to tumorigenesis have been unclear. Here, we show that expression of NUP98 fusion oncoproteins causes mitotic spindle defects and chromosome missegregation, correlating with the capability of NUP98 fusions to cause premature securin degradation and slippage from an unsatisfied spindle assembly checkpoint (SAC). NUP98 fusions, unlike wild-type NUP98, were found to physically interact with the anaphase promoting complex/cyclosome (APC/C)(Cdc20) and to displace the BubR1 SAC component, suggesting a possible mechanistic basis for their interference with SAC function. In addition, NUP98 oncoproteins displayed a prolonged half-life in cells. We found that NUP98 stability is controlled by a PEST sequence, absent in NUP98 oncoproteins, whose deletion reproduced the aberrant SAC-interfering activity of NUP98 oncoproteins. Together, our findings suggest that NUP98 oncoproteins predispose myeloid cells to oncogenic transformation or malignant progression by promoting whole chromosome instability.