methylnitronitrosoguanidine and Fish-Diseases

Of 158 channel catfish (Ictalurus punctatus) exposed to N-methyl-N'-nitro-N-nitrosoguanidine [(MNNG) CAS:70-25-7] in water for 28 days, 2 developed disseminated lymphosarcoma. One fish was necropsied at 12 months and another at 18 months following exposure. Both fish had a massive neoplastic infiltration of the bilateral pairs of head and trunk kidneys from which the neoplastic cells appeared to originate. The neoplastic infiltration was also observed in the following: thymus, gills, oral mucosa, liver, skin, skeletal muscle of head-neck region, and to a lesser extent spleen and bone marrow. This is probably the first report of lymphosarcoma in channel catfish. Although the occurrence of lymphosarcoma in these 2 catfish appeared to be related to exposure to MNNG, the exact role MNNG played in the tumor formation was not determined.

Topics: Animals; Carcinoma; Carcinoma, Squamous Cell; Fish Diseases; Fishes; Kidney Neoplasms; Lipoma; Lymphoma, Non-Hodgkin; Methylnitronitrosoguanidine; Mouth Mucosa; Mouth Neoplasms; Papilloma; Water Pollutants, Chemical

Juvenile medaka were exposed to N-methyl-N'-nitro-N-nitrosoguanidine in water under static renewal conditions for 28 days. Two groups of 134 fish each were pulsed 3 times weekly at nominal concentrations of 1.0 and 0.5 mg/liter with N-methyl-N'-nitro-N-nitrosoguanidine dissolved in dimethylformamide. A third group of 134 fish was exposed to the solvent control, 0.01% dimethylformamide in water. Following the 28-day exposure, and during the recovery period, fish were sampled at intervals of approximately 0, 3, 6, and 9 months and examined grossly. Selected tissues were evaluated microscopically. Many tumor types developed in both N-methyl-N'-nitro-N-nitrosoguanidine exposure groups, but only the gill lesions will be discussed. Approximately 50% of the fish in both treatment groups died from gill damage in the second to third month of the recovery period. More than 90% of the surviving treated fish displayed gill lesions, which progressed from mild epithelial hyperplasia of gill filaments at 0-months recovery to epitheliomatous hyperplasia at 3 months and advanced to a more focal nodular appearance of gill filaments at 6 months. Eight to 9 months after the treatment period, at least four fish displayed branchial blastomas. The control fish had no gill lesions. Chemically induced gill tumors have not been previously observed in fish. Even gill tumors of unknown origin are very rare.

Topics: Animals; Disease Models, Animal; Fish Diseases; Fishes; Gills; Hyperplasia; Methylnitronitrosoguanidine; Neoplasms; Time Factors

Chromatophoromas in the croaker nibe, Nibea mitsukurii, are common neoplasms in feral fish which inhabit the shallow water in a unique geographic distribution along the Pacific coast of Japan. We undertook surveys of the epizootiology of tumor-bearing fish at 25 sites. The highest tumor incidence occurred at the station near the mouth of the Kumano river and was 47% (1,415 of 2,991). The incidence at 2 adjacent survey stations located approximately 18 and 30 km away were 2.7 and 2.5%, respectively. At the other survey stations, no tumor incidences were recorded or they were less than 5%. During the course of experimental studies on the chromatophoromas using tank-reared nibe, we found that nifurpirinol (NP), a drug used for the treatment of fish diseases, might also induce the chromatophoromas in the fish, as well as N-methyl-N'-nitro-N-nitrosoguanidine and 7,12-dimethylbenz[alpha]anthracene. Therefore, tank-reared nibe 5 months of age were divided into 4 groups of about 50 each and exposed to water containing 0, 0.5, 1, or 2 ppm NP, respectively, fourteen times for 1 hour each time. Three hundred nibe were kept as untreated controls. The incidences of chromatophore hyperplasia or neoplasia per group at 13 months were as follows: the untreated: 2.9% (6 of 204), 0 ppm: 5.3% (2 of 38), 0.5 ppm: 73% (36 of 49), 1 ppm: 87% (20 of 23), and 2 ppm: 100% (2 of 2). These and other results led us to believe that 1) NP is a carcinogen, 2) nibe have a high susceptibility to induction of chromatophoromas by chemical carcinogens, and 3) some environmental chemicals are causal factors in the hyperendemic occurrences of the tumors in wild nibe.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Carcinogens, Environmental; Female; Fish Diseases; Fishes; Male; Melanoma; Methylnitronitrosoguanidine; Mice; Mice, Inbred ICR; Mutagenicity Tests; Nitrofurans; Sex Factors