allopurinol and Fish-Diseases

Adenosine deaminase (ADA) activity, through adenosine (Ado) levels, as well as xanthine oxidase (XO) activity through uric acid levels exerts an essential role on immune and inflammatory responses during infectious diseases. Thus, the aim of this study was to evaluate the involvement of seric ADA and XO activities in the inflammatory and oxidative status of silver catfish naturally infected with Ichthyophthirius multifiliis. Seric ADA activity decreased, while Ado levels increased in infected animals compared to uninfected animals. Moreover, the seric XO activity increased in infected animals compared to uninfected animals, alongside the seric levels of uric acid, metabolites of nitric oxide (NOx) and reactive oxygen species (ROS). Based on this evidence, the downregulation of seric ADA activity exerts an anti-inflammatory profile, contributing to restricting the inflammatory process. The most important finding is that upregulation of seric XO activity leads to an excessive formation of uric acid, which contributes to oxidative and inflammatory processes. Moreover, uric acid induces the release of pro-inflammatory and pro-oxidative mediators, such NOx and ROS, which contribute directly to disease pathogenesis. In summary, the upregulation of XO activity may be considered a pathway involved in NOx and ROS production in silver catfish infected with I. multifiliis.

Topics: Adenosine Deaminase; Animals; Catfishes; Ciliophora Infections; Fish Diseases; Fish Proteins; Hymenostomatida; Inflammation; Oxidative Stress; Xanthine Oxidase

Nanoencapsulated Melaleuca alternifolia essential oil (tea tree oil, TTO) is a natural alternative treatment, with 100% therapeutic efficacy in fish experimentally infected with Pseudomonas aeruginosa, and has also potent protective effects linked with antioxidant properties. However, the pathways responsible for the antioxidant capacity remain unknown. Thus, this study evaluated whether the inhibition of seric xanthine oxidase (XO) activity can be considered a pathway involved in the antioxidant capacity of nanoencapsulated TTO in fish experimentally infected with P. aeruginosa. Seric samples from fish infected with P. aeruginosa showed increased XO activity, as well as increased uric acid and reactive oxygen species (ROS) levels. In contrast, the prophylactic treatment with nanoencapsulated TTO prevented these infection-induced alterations. Based on the evidence obtained, the upregulation of seric XO activity induced pro-oxidative effects in the serum of fish experimentally infected with P. aeruginosa, due to excessive formation of uric acid, which stimulates the release of ROS. This treatment was able to prevent the upregulated seric XO activity and, consequently, the excessive formation of uric acid and ROS. In summary, inhibition of seric XO activity can be considered a pathway involved in the antioxidant capacity of nanoencapsulated TTO in fish experimentally infected with P. aeruginosa.

Topics: Animals; Anti-Bacterial Agents; Antioxidants; Catfishes; Fish Diseases; Fish Proteins; Nanocapsules; Pseudomonas aeruginosa; Pseudomonas Infections; Tea Tree Oil; Xanthine Oxidase

Several studies have associated the involvement of xanthine oxidase (XO) activity, a source of uric acid and reactive oxygen species (ROS), to pro-oxidative and pro-inflammatory effects during pathological conditions. Considering this, the aim of this study was to evaluate whether upregulation on seric XO activity may be a pathway involved in the oxidative stress in fish exposed to a diet contaminated with aflatoxin B

Topics: Aflatoxin B1; Animals; Catfishes; Diet; Fish Diseases; Fish Proteins; Food Contamination; Inflammation; Nitrogen Oxides; Oxidative Stress; Reactive Oxygen Species; Up-Regulation; Xanthine Oxidase

Several pieces of evidence have linked the involvement of xanthine oxidase (XO), a source of uric acid and reactive oxygen species (ROS), to pro-oxidative and pro-inflammatory effects observed during bacterial fish diseases. Thus, the aim of this study was to evaluate whether upregulation of splenic XO activity contributes to disease pathogenesis of Aeromonas caviae infection, as well as whether it may be considered a pathway involved in ROS and nitric oxide (NO) production. XO activity increased in the spleen of infected animals, as did the splenic levels of uric acid, ROS and metabolites of nitric oxide (NOx), compared to the uninfected control group. Based on this evidence, upregulation of splenic XO activity induces pro-oxidant and pro-inflammatory profiles in the spleen of fish infected by A. caviae due to excessive formation of uric acid. Moreover, excessive uric acid induces the release of pro-inflammatory mediators, such as ROS and NOx, which contribute to disease pathophysiology. In summary, upregulation of XO activity may be considered a pathway involved in ROS and NOx production.

Topics: Aeromonas caviae; Animals; Catfishes; Fish Diseases; Gram-Negative Bacterial Infections; Inflammation; Nitric Oxide; Oxidation-Reduction; Oxidative Stress; Spleen; Uric Acid; Xanthine Oxidase

In vivo infection studies in Japanese flounder (Paralichthys olivaceus) demonstrated that the number of viable cells of the virulent strain (NUF251) of Edwardsiella tarda increased gradually in kidney and hepato-pancreas after intraperitoneal injection, but the low virulent strain (NUF194) did not. To gain insight into the virulence factors of E. tarda, in vitro responses of Japanese flounder (P. olivaceus) peritoneal macrophages to these strains were compared in terms of phagocytosis, bactericidal activity, and reactive oxygen species (ROS) generation as measured by chemiluminescence (CL) responses. Microscopic observation revealed that these two strains of E. tarda were phagocytosed by the peritoneal macrophages, and there was no significant difference in the mean numbers of ingested bacteria per macrophage between these strains. A gradual increase in the number of viable cells of the highly virulent strain within macrophages was observed during 9h post-phagocytosis, whereas no significant replication of the low virulent strain within macrophages was detected. These results suggest that the virulent strain of E. tarda has an ability to survive and replicate within macrophages, while the low virulent strain has no such ability. When the peritoneal macrophages were exposed to the opsonized low virulent E. tarda strain, a rapid increase in CL response was induced. However, the highly virulent strain caused only background level of CL response. By the subsequent stimulation with phorbol myristate acetate, the macrophages exposed to the virulent E. tarda strain showed extremely higher CL response than that of the one exposed to the low virulent E. tarda strain. These results suggest that the virulent E. tarda prevents the activation of ROS generation system during phagocytosis, though the system is still capable of responding to other stimulation. The virulent strain significantly reduced the CL response induced by xanthine/xanthine oxidase system, while the low virulent strain had almost no effect. Furthermore, the virulent strain showed greater resistance to H(2)O(2) than the low virulent strain. Our results suggest that the virulent strain of E. tarda is highly resistant to ROS, and such ability might allow the organism to survive and multiply within phagocytes, and may serve to disseminate E. tarda throughout the host during in vivo infection.

Topics: Animals; Anti-Bacterial Agents; Blood Bactericidal Activity; Carcinogens; Colony Count, Microbial; Edwardsiella tarda; Enterobacteriaceae Infections; Fish Diseases; Flounder; Gentamicins; Hydrogen Peroxide; Luminescence; Macrophages, Peritoneal; Oxidants; Phagocytosis; Reactive Oxygen Species; Tetradecanoylphorbol Acetate; Time Factors; Xanthine Oxidase