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M T Santamarina - One of the best experts on this subject based on the ideXlab platform.
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Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. II: Gyrodactylus sp.
Diseases of Aquatic Organisms, 1998Co-Authors: J. L. Tojo, M T SantamarinaAbstract:A total of 24 drugs were evaluated as regards their efficacy for oral treatment of gyrodactylosis in rainbow trout Oncorhynchus mykiss. In preliminary trials, all drugs were supplied to infected fish at 40 g per kg of feed for 10 d. Twenty-two of the drugs tested (aminosidine, amprolium, benznidazole, bithionol, chloroquine, diethylcarbamazine, flubendazole, levamisole, mebendazole, metronidazole, niclosamide, nitroxynil, oxibendazole, parbendazole, piperazine, praziquantel, ronidazole, secnidazole, tetramisole, thiophanate, toltrazuril and trichlorfon) were ineffective. Triclabendazole and Nitroscanate completely eliminated the infection. Triclabendazole was effective only at the screening dosage (40 g per kg of feed for 10 d), while Nitroscanate was effective at dosages as low as 0.6 g per kg of feed for 1 d.
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Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. III: Ichthyobodo necator
Diseases of Aquatic Organisms, 1998Co-Authors: J. L. Tojo, M T SantamarinaAbstract:A total of 32 drugs were evaluated as regards their efficacy for oral treatment of Ichthyobodo necator infestation of rainbow trout. In preliminary trials, all drugs were supplied to infected fish at 40 g per kg of feed for 10 d. The majority of the drugs tested (1,3-di-6-quinolylurea, aminosidine, amprolium, benznidazole, bithionol, chloroquine, diethylcarbamazine, dimetridazole, diminazene aceturate, febantel, flubendazole, ketoconazole, levamisole, mebendazole, netobimin, niclosamide, niridazole, Nitroscanate, nitroxynil, oxibendazole, parbendazole, piperazine, praziquantel, ronidazole, sulphaquinoxaline, tetramisole, thiophanate, toltrazuril and trichlorfon) were ineffectdive. Metronidazole and secnidazole were 100% effective (unlike the other nitroimidazoles tested, namely dimetridazole, benznidazole and ronidazole). The non-carbamate benzimidazole triclabendazole was likewise 100% effective.
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Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. I: Hexamita salmonis
Diseases of Aquatic Organisms, 1998Co-Authors: J. L. Tojo, M T SantamarinaAbstract:Abstract Various drugs were evaluated as regards efficacy for the treatment of Hexamita salmonis infection in rainbow trout. The results confirm the efficacy of nitroimidazoles: infection was completely eradicated not only by metronidazole (which has been recommended previously for the treatment of hexamitosis), but also by benznidazole, ronidazole and secnidazole, which have not been assayed previously. The non-nitroimidazoles albendazole, aminosidine, diethylcarbamazine and Nitroscanate also completely eliminated infection. The remaining non-nitroimidazoles tested (amprolium, bithionol, febantel, flubendazole, levamisole, netobimin, niclosamide, nitroxynil, oxibendazole, parbendazole, piperazine, praziquentel, tetramisole, thiophanate, toltrazuril, trichlorfon and triclabendazole) were not effective.
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Anthelmintic treatment against Gyrodactylus sp. infecting rainbow trout Oncorhynchus mykiss
Diseases of Aquatic Organisms, 1991Co-Authors: M T Santamarina, J. Tojo, Florencio M. Ubeira, P. Quinteiro, M. L. SanmartínAbstract:Various anthelmintics belonging to different pharmacological groups (ivermectin, clorsulon, closantel, netobimin, febantel, praziquantel, niclofolan, bithionol, trichlorfon, levamisole hydrochloride, piperazine citrate and dihydrochloride, Nitroscanate), all of proven efficacy against certain helminths, were tested and compared for their in vivo and in vitro activity on a natural infection of Oncorhynchus mykiss by Gyrodactylus, probably G. salaris. The trout were also observed for signs of toxic reaction to the drugs. Complete efficacy (100 % reduction) with no toxic effects was achieved only by bithionol (20 mg I-') and Nitroscanate (0.07 mg 1-l).
T.r. Juneja - One of the best experts on this subject based on the ideXlab platform.
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Mutagenicity of sulfoscanate: a comparative study.
Mutation research, 2002Co-Authors: T.r. Juneja, Arindam Talukdar, R.l. GuptaAbstract:The mutagenic activity of sulfoscanate (SSC) (4-isothiocyanate-4'-nitrodiphenyl sulphide) has been compared with that of the following reported drugs: (a) Nitroscanate (NSC) (4-isothiocyanate-4'-nitrodiphenyl ether) which is a veterinary anthelmintic drug and (b) amoscanate (ASC) (4-isothiocyanate-4'-nitrodiphenyl amine) which is effective against schistosomes. SSC has been found to be a very potent mutagen towards TA98 and TA100 inducing 26.0 and 475.5revertants/nmole, respectively. NSC was found to induce mutations at a rate of 11.1 and 21.5revertants/nmole in TA98 and TA100, respectively. ASC was found to be non-mutagenic as such, but the urine of animals given the drug displayed mutagenicity. When SSC was tested in TA98/1,8-DNP(6), deficient in O-acetyltransferase, the activity decreased to 10.0revertants/nmole. However, in case of NSC the mutagenic activity was reduced to 0.24revertants/nmole, indicating the importance of O-acetyltransferase in generating N-acetoxyarylamine. In TA98NR, deficient in nitroreductase, the mutagenicity of SSC and NSC was totally absent. The positional isomers of SSC, 4-isothiocyanate-3'-nitro- and 4-isothiocyanate-2'-nitrodiphenyl sulphide, were found to be non-mutagenic in both TA98 and TA100. Our comparison of the mutagenic activity of SSC, NSC and ASC indicates that the pattern of activity is SSC>NSC>ASC.
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Genotoxicity of potential metabolites of Nitroscanate--an antischistosomal drug.
Mutation research, 1995Co-Authors: R.l. Gupta, Indu Pal Kaur, T.r. JunejaAbstract:Abstract The potential metabolites of Nitroscanate(4-isothiocyanato-4′-nitrodiphenyl ether) such as 4-amino-4′-nitrodiphenyl ether (ANDE), 4-acetamido -4″-nitrodiphenyl ether (AcNDE), 4-acetamido-4′-nitrosodiphenyl ether (4-N = 0), 4-acetamido-4′- hydroxylaminodiphenyl ether (4-NHOH), 4-acetamido-4′-acetohydroxamicdiphenyl ether [4-N(OH)AC], 4-acetamido-4′-for-mohydroxamicdiphenyl ether [4-N(OH)CHO] and 4-acetamido-4′-acetylaceto-hydroxamicdiphenyl ether [4-N(OAc)Ac] were synthesized and investigated in the standard Salmonella mutagenicity test using TA98, TA98NR, TA98/1,8-DNP 6 , TA100 and TA100NR as indicator strains, in the presence and absence of hepatic S9. The relative order of activity among nitro and its reduction products, 4-N =0 and 4-NHOH in TA98 and TA100 was 4-N - 0 > 4-NHOH > AcNDE. In nitroreductase deficient strain TA98NR, AcNDE was inactive, but expressed a slight activity in TA100NR while 4-N =0 and 4-NHOH showed a large increase in specific activity in both the strains. In O-acetyltransferase deficient strain TA98/1,8-DNP 6 , AcNDE was inactive, while 4-N = 0 and 4-NHOH showed a sharp fall inactivity. The hydroxylamine derived products with an activity order 4-N(OAc)Ac > 4-N(OH)CHO > 4-N(OH)Ac in both TA98 and TA100, showed 3–6 times increase in the specific activity for the latter two compounds in the presence of S9 mix, which was inhibited in the presence of paraoxan, indicating N-deacylation as an important metabolic activation pathway. Except the 4-NO in TA100, the observed mutagenicity of nitroscante (NSC) was higher than those of potential metabolites and the nor-isothiocyanato derivative 4′-nitrodiphenyl ether, thereby showing that -NCS function has a potentiating effect on the mutagenicity of this drug.
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Mutagenicity of Nitroscanate, an antischistosomal drug
Mutation research, 1995Co-Authors: R.l. Gupta, Indu Pal Kaur, T.r. JunejaAbstract:Nitroscanate (NSC) was found to be a direct acting mutagen in the Ames Salmonella tester strains TA100 and TA98 and this activity increased further in the presence of rat liver S9 mix. It was inactive in TA98NR and TA100NR, and weakly active in TA98/1,8-DNP6. A substantial fall in drug induced mutagenicity by pentachlorophenol, an inhibitor of acetyltransferase, in TA98, TA100 and YG1024 suggests the initial bioconversion of a nitro group to hydroxylamine and its further activation to the ultimate N-acetoxyarylamine. The refrigerated DMSO solution of the drug in the plate incorporation assay and freshly prepared solutions using the pre-incubation procedure indicated a fall in mutagenicity owing to the conversion of NSC to N,N'-bis-4-(p-nitrophenoxy)phenyl thiourea (NFPT). The drastic reduction in mutagenicity in the presence of 4-amino-4'-nitrodiphenyl ether (ANDE) and 4-aminodiphenyl ether (ADE) was also attributed to the conversion of NSC to the corresponding thiourea, a non-mutagen. The negligible mutagenicity of ANDE and its absence in ADE and 4-isothiocyanate diphenyl ether (ITDE) suggests that the mutagenicity of NSC is due to the nitro group, and the -NCS function is responsible for enhanced mutagenicity over nor-isothiocyanate 4-nitrodiphenyl ether (NDE).
J. L. Tojo - One of the best experts on this subject based on the ideXlab platform.
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Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. II: Gyrodactylus sp.
Diseases of Aquatic Organisms, 1998Co-Authors: J. L. Tojo, M T SantamarinaAbstract:A total of 24 drugs were evaluated as regards their efficacy for oral treatment of gyrodactylosis in rainbow trout Oncorhynchus mykiss. In preliminary trials, all drugs were supplied to infected fish at 40 g per kg of feed for 10 d. Twenty-two of the drugs tested (aminosidine, amprolium, benznidazole, bithionol, chloroquine, diethylcarbamazine, flubendazole, levamisole, mebendazole, metronidazole, niclosamide, nitroxynil, oxibendazole, parbendazole, piperazine, praziquantel, ronidazole, secnidazole, tetramisole, thiophanate, toltrazuril and trichlorfon) were ineffective. Triclabendazole and Nitroscanate completely eliminated the infection. Triclabendazole was effective only at the screening dosage (40 g per kg of feed for 10 d), while Nitroscanate was effective at dosages as low as 0.6 g per kg of feed for 1 d.
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Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. III: Ichthyobodo necator
Diseases of Aquatic Organisms, 1998Co-Authors: J. L. Tojo, M T SantamarinaAbstract:A total of 32 drugs were evaluated as regards their efficacy for oral treatment of Ichthyobodo necator infestation of rainbow trout. In preliminary trials, all drugs were supplied to infected fish at 40 g per kg of feed for 10 d. The majority of the drugs tested (1,3-di-6-quinolylurea, aminosidine, amprolium, benznidazole, bithionol, chloroquine, diethylcarbamazine, dimetridazole, diminazene aceturate, febantel, flubendazole, ketoconazole, levamisole, mebendazole, netobimin, niclosamide, niridazole, Nitroscanate, nitroxynil, oxibendazole, parbendazole, piperazine, praziquantel, ronidazole, sulphaquinoxaline, tetramisole, thiophanate, toltrazuril and trichlorfon) were ineffectdive. Metronidazole and secnidazole were 100% effective (unlike the other nitroimidazoles tested, namely dimetridazole, benznidazole and ronidazole). The non-carbamate benzimidazole triclabendazole was likewise 100% effective.
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Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. I: Hexamita salmonis
Diseases of Aquatic Organisms, 1998Co-Authors: J. L. Tojo, M T SantamarinaAbstract:Abstract Various drugs were evaluated as regards efficacy for the treatment of Hexamita salmonis infection in rainbow trout. The results confirm the efficacy of nitroimidazoles: infection was completely eradicated not only by metronidazole (which has been recommended previously for the treatment of hexamitosis), but also by benznidazole, ronidazole and secnidazole, which have not been assayed previously. The non-nitroimidazoles albendazole, aminosidine, diethylcarbamazine and Nitroscanate also completely eliminated infection. The remaining non-nitroimidazoles tested (amprolium, bithionol, febantel, flubendazole, levamisole, netobimin, niclosamide, nitroxynil, oxibendazole, parbendazole, piperazine, praziquentel, tetramisole, thiophanate, toltrazuril, trichlorfon and triclabendazole) were not effective.
R.l. Gupta - One of the best experts on this subject based on the ideXlab platform.
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Mutagenicity of sulfoscanate: a comparative study.
Mutation research, 2002Co-Authors: T.r. Juneja, Arindam Talukdar, R.l. GuptaAbstract:The mutagenic activity of sulfoscanate (SSC) (4-isothiocyanate-4'-nitrodiphenyl sulphide) has been compared with that of the following reported drugs: (a) Nitroscanate (NSC) (4-isothiocyanate-4'-nitrodiphenyl ether) which is a veterinary anthelmintic drug and (b) amoscanate (ASC) (4-isothiocyanate-4'-nitrodiphenyl amine) which is effective against schistosomes. SSC has been found to be a very potent mutagen towards TA98 and TA100 inducing 26.0 and 475.5revertants/nmole, respectively. NSC was found to induce mutations at a rate of 11.1 and 21.5revertants/nmole in TA98 and TA100, respectively. ASC was found to be non-mutagenic as such, but the urine of animals given the drug displayed mutagenicity. When SSC was tested in TA98/1,8-DNP(6), deficient in O-acetyltransferase, the activity decreased to 10.0revertants/nmole. However, in case of NSC the mutagenic activity was reduced to 0.24revertants/nmole, indicating the importance of O-acetyltransferase in generating N-acetoxyarylamine. In TA98NR, deficient in nitroreductase, the mutagenicity of SSC and NSC was totally absent. The positional isomers of SSC, 4-isothiocyanate-3'-nitro- and 4-isothiocyanate-2'-nitrodiphenyl sulphide, were found to be non-mutagenic in both TA98 and TA100. Our comparison of the mutagenic activity of SSC, NSC and ASC indicates that the pattern of activity is SSC>NSC>ASC.
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Genotoxicity of potential metabolites of Nitroscanate--an antischistosomal drug.
Mutation research, 1995Co-Authors: R.l. Gupta, Indu Pal Kaur, T.r. JunejaAbstract:Abstract The potential metabolites of Nitroscanate(4-isothiocyanato-4′-nitrodiphenyl ether) such as 4-amino-4′-nitrodiphenyl ether (ANDE), 4-acetamido -4″-nitrodiphenyl ether (AcNDE), 4-acetamido-4′-nitrosodiphenyl ether (4-N = 0), 4-acetamido-4′- hydroxylaminodiphenyl ether (4-NHOH), 4-acetamido-4′-acetohydroxamicdiphenyl ether [4-N(OH)AC], 4-acetamido-4′-for-mohydroxamicdiphenyl ether [4-N(OH)CHO] and 4-acetamido-4′-acetylaceto-hydroxamicdiphenyl ether [4-N(OAc)Ac] were synthesized and investigated in the standard Salmonella mutagenicity test using TA98, TA98NR, TA98/1,8-DNP 6 , TA100 and TA100NR as indicator strains, in the presence and absence of hepatic S9. The relative order of activity among nitro and its reduction products, 4-N =0 and 4-NHOH in TA98 and TA100 was 4-N - 0 > 4-NHOH > AcNDE. In nitroreductase deficient strain TA98NR, AcNDE was inactive, but expressed a slight activity in TA100NR while 4-N =0 and 4-NHOH showed a large increase in specific activity in both the strains. In O-acetyltransferase deficient strain TA98/1,8-DNP 6 , AcNDE was inactive, while 4-N = 0 and 4-NHOH showed a sharp fall inactivity. The hydroxylamine derived products with an activity order 4-N(OAc)Ac > 4-N(OH)CHO > 4-N(OH)Ac in both TA98 and TA100, showed 3–6 times increase in the specific activity for the latter two compounds in the presence of S9 mix, which was inhibited in the presence of paraoxan, indicating N-deacylation as an important metabolic activation pathway. Except the 4-NO in TA100, the observed mutagenicity of nitroscante (NSC) was higher than those of potential metabolites and the nor-isothiocyanato derivative 4′-nitrodiphenyl ether, thereby showing that -NCS function has a potentiating effect on the mutagenicity of this drug.
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Mutagenicity of Nitroscanate, an antischistosomal drug
Mutation research, 1995Co-Authors: R.l. Gupta, Indu Pal Kaur, T.r. JunejaAbstract:Nitroscanate (NSC) was found to be a direct acting mutagen in the Ames Salmonella tester strains TA100 and TA98 and this activity increased further in the presence of rat liver S9 mix. It was inactive in TA98NR and TA100NR, and weakly active in TA98/1,8-DNP6. A substantial fall in drug induced mutagenicity by pentachlorophenol, an inhibitor of acetyltransferase, in TA98, TA100 and YG1024 suggests the initial bioconversion of a nitro group to hydroxylamine and its further activation to the ultimate N-acetoxyarylamine. The refrigerated DMSO solution of the drug in the plate incorporation assay and freshly prepared solutions using the pre-incubation procedure indicated a fall in mutagenicity owing to the conversion of NSC to N,N'-bis-4-(p-nitrophenoxy)phenyl thiourea (NFPT). The drastic reduction in mutagenicity in the presence of 4-amino-4'-nitrodiphenyl ether (ANDE) and 4-aminodiphenyl ether (ADE) was also attributed to the conversion of NSC to the corresponding thiourea, a non-mutagen. The negligible mutagenicity of ANDE and its absence in ADE and 4-isothiocyanate diphenyl ether (ITDE) suggests that the mutagenicity of NSC is due to the nitro group, and the -NCS function is responsible for enhanced mutagenicity over nor-isothiocyanate 4-nitrodiphenyl ether (NDE).
M. L. Sanmartín - One of the best experts on this subject based on the ideXlab platform.
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Anthelmintic treatment against Gyrodactylus sp. infecting rainbow trout Oncorhynchus mykiss
Diseases of Aquatic Organisms, 1991Co-Authors: M T Santamarina, J. Tojo, Florencio M. Ubeira, P. Quinteiro, M. L. SanmartínAbstract:Various anthelmintics belonging to different pharmacological groups (ivermectin, clorsulon, closantel, netobimin, febantel, praziquantel, niclofolan, bithionol, trichlorfon, levamisole hydrochloride, piperazine citrate and dihydrochloride, Nitroscanate), all of proven efficacy against certain helminths, were tested and compared for their in vivo and in vitro activity on a natural infection of Oncorhynchus mykiss by Gyrodactylus, probably G. salaris. The trout were also observed for signs of toxic reaction to the drugs. Complete efficacy (100 % reduction) with no toxic effects was achieved only by bithionol (20 mg I-') and Nitroscanate (0.07 mg 1-l).