Data/hora: 01/06/2024 06:16:22

Provedor de dados: 	42	
País: 	Brazil	
Título: 	Oxidative stress and fish immune system: phagocytosis and leukocyte respiratory burst activity	
Autores: 	BILLER,JAQUELINE D.; TAKAHASHI,LEONARDO S.	
Data: 	2018-12-01	
Ano: 	2018	
Palavras-chave: 	Reactive oxygen species; Innate immunity; Antioxidant system; Free radical.	
Resumo: 	Abstract Molecular oxygen is a necessary compound for all aerobic organisms, although oxygen is a potent oxidant, which can cause oxidative stress (OS). OS occurs when there is an imbalance between the production of oxidant and antioxidants components, are result of normal cell metabolism, and many of these compounds play a fundamental role in several metabolic pathways. The organism produces several reactive oxygen species (ROS), but they are balanced by an antioxidant defense system that maintains the levels of these oxidizing compounds at an acceptable level. Many of these components are essential in the organism defense and their byproducts are considered potent bactericides that actively act in the destruction of invading pathogens. Fish immune system is composed of innate and acquired mechanisms of defense. Phagocytosis is an innate process of defense, which interconnects these two systems, since the pathogens processing by professional phagocytes is a fundamental stage for antibodies production. During phagocytosis there is production of ROS and consequent production of free radicals (FR), these compounds lead to the formation of potent bactericides to combat microorganisms. However, it is known that OS limits the immune response, with an impairment in defense compounds in an attempt to decrease the ROS production. Studies of fish FR production are preliminary and should be executed to evaluate the effects of ROS on fish, including their beneficial action against pathogens and its deleterious action on the oxidation of cellular components.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652018000703403	
Editor: 	Academia Brasileira de Ciências	
Relação: 	10.1590/0001-3765201820170730	
Formato: 	text/html	
Fonte: 	Anais da Academia Brasileira de Ciências  v.90 n.4 2018	
Fonte: 	info:eu-repo/semantics/openAccess