RESUMO
The objective of this study was to investigate the effects of riboflavin-deficient and Trichinella spiralis-induced stresses on corticosterone associated with spermatogenesis in male Wistar rats. Rats were allocated into 4 groups: Group 1: control; group 2: riboflavin-deficient diet; group 3: T. spiralis infection; group 4: riboflavin deficient diet with T. spiralis infection. This experiment lasted for 12 weeks. Plasma corticosterone was significantly enhanced when exposed to acute riboflavin deficiency and/or T. spiralis infection stress. When the rats were chronically subjected to such stresses, T. spiralis per se had prolonged effects, in a marked increase in corticosterone. T. spiralis per se tended to impact on such sperm characteristics as sperm motility, sperm count and daily sperm production, even defected seminiferous tubules. It was proposed that the Trichinella spiralis-induced stress probably had adverse effects on the level of adrenocortical-testicular axis whenever their habitats on muscle fibers were evident. However, riboflavin-deficient-induced stress had little implication in the adrenocortical-testicular axis.
Assuntos
Fenômenos Fisiológicos da Nutrição Animal , Animais , Corticosterona/sangue , Modelos Animais de Doenças , Masculino , Distribuição Aleatória , Ratos , Ratos Wistar , Deficiência de Riboflavina/sangue , Túbulos Seminíferos/patologia , Contagem de Espermatozoides , Motilidade dos Espermatozoides , Espermatogênese/fisiologia , Trichinella spiralis , Triquinelose/sangueRESUMO
The erythrocyte antioxidant enzyme levels of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) of riboflavin-deficient and Trichinella spiralis-infected rats were investigated. The rats were deprived of riboflavin at the 8th week of the experiment. At that time, the erythrocyte glutathione reductase activity coefficient (EGR AC), as an indicator of riboflavin status, was > or = 1.30 in rats fed a riboflavin-deficient diet and T. spiralis-infected rats fed a riboflavin-deficient diet showed no biochemical sign of riboflavin deficiency. At the 12th week of the experiment, the levels of catalase, SOD and GSH-Px were significantly lower in the riboflavin-deficient, T. spiralis-infected, and combined riboflavin-deficient and T. spiralis-infected, rats, compared to the control group. This may have been due to an increase in free oxygen radicals caused by riboflavin deficiency and parasitic infection.