ABSTRACT
Ciguatera poisoning (CP) is a foodborne disease known for centuries; however, little research has been conducted on the effects of ciguatoxins (CTXs) on fish metabolism. The main objective of this study was to assess different hepatic compounds observed in goldfish (Carassius auratus) fed C-CTX1 using nuclear magnetic resonance (NMR)-based metabolomics. Thirteen goldfish were treated with C-CTX1-enriched flesh and sampled on days 1, 8, 15, 29, 36, and 43. On day 43, two individuals, referred to as 'Detox', were isolated until days 102 and 121 to evaluate the possible recovery after returning to a commercial feed. At each sampling, hepatic tissue was weighed to calculate the hepatosomatic index (HSI) and analyzed for the metabolomics study; animals fed toxic flesh showed a higher HSI, even greater in the 'Detox' individuals. Furthermore, altered concentrations of alanine, lactate, taurine, glucose, and glycogen were observed in animals with the toxic diet. These disturbances could be related to an increase in ammonium ion (NH4+) production. An increase in ammonia (NH3) concentration in water was observed in the aquarium where the fish ingested toxic meat compared to the non-toxic aquarium. All these changes may be rationalized by the relationship between CTXs and the glucose-alanine cycle.
ABSTRACT
Motivo y objetivos: El rugby es un deporte de contacto de gran popularidad en el mundo donde el jugador sufre impactos que pueden acontecer con traumas músculo-esqueléticos. La sensibilización central es un aumento de respuesta de las neuronas centrales a señales provenientes de los receptores unimodales y polimodales. Por tanto, puede ser generada desde la periferia mediante señales nociceptivas prolongadas en el tiempo. Material y métodos: Muestra de 30 jugadores de rugby (15 mujeres y 15 hombres) con dolor músculo-esquelético sub-agudo o crónico, originado de la práctica deportiva y un grupo control que no presentaban dolor. Se midió bilateralmente el umbral de dolor a la presión en la articulación acromio-clavicular; nervio mediano; nervio cubital; segundo metacarpiano; músculotibial anterior; ligamento peroneo-astragalino anterior; articulación C5/6; músculo infraespinoso y apófisis espinosa de L3. Resultados: El 52% presentaban dolor músculo-esquelético. La duración media del dolor fue de 27,5 ± 11,1 semanas, la intensidad media de dolor en la última semana de 4,1 ± 1,7; la intensidad máxima de 6 ± 1,9; y la intensidad mínima de 1,8 ± 1,2. El ANOVA no encontró diferencias significativas en los umbrales de dolor a la presión en ninguno de los puntos analizados entre jugadores de rugby con y sin dolor (P > 0,05). Discusión: El cuestionario revela que el dolor que padecen se produce durante la práctica deportiva, y no interfiere en actividades de la vida diaria. No se han encontrado signos de sensibilización tanto periférica como central en jugadores con dolor músculo-esquelético. Podría deberse, a la disparidad de lesiones que presentaban los deportistas, o bien, por la dificultad existente para evaluar la percepción de dolor en deportistas
Background and objective: Rugby is a famous contact sport around the world where the player can receive impacts accounting for musculo-skeletal trauma. Central sensitization represents an increased response of the neurons of the central nervous system originated from continuous afferent nociceptive inputs from peripheral tissues. Material and methods: Thirty rugby players (15 men, 15 women) participated in this study. They were divided into those with acute or chronic musculoskeletal pain originated from the sport practice and into a control group formed for those without pain. Pressure pain thresholds (PPT) were bilaterally assessed over the acromio-clavicular joint, median nerve, ulnarnerve, second metacarpal, tibialis anterior muscle, anterior talofibular ligament, C5/C6 joint, infraspinatus muscle and spinous process of L3. Results: Fifty-two percent (n=16) of rugby players exhibited pain. The mean duration of pain was 27.5 ± 11.1 weeks, mean pain intensity experienced the previous week was 4.1 ± 1.7, the worst pain intensity was 6 ±1.9, and the lowest pain intensity was 1.8 ± 1.2). The ANOVA test did not reveal significant differences in pressure pain thresholds in any of the analyzed points between rugby player with and without pain (P > 0.05). Discussion: Our results suggest that rugby players exhibited musculoskeletal pain derived from the sport but the pain does not inferred into daily life activities. The current study did not show the presence of peripheral or central sensitization mechanism in rugby players suffering musculoskeletal pain. Current results can be related to the different lesions and pain areas that the participants included in our study suffered from, and/or also to differences in pain perception in sport players in general
