Biochemical Markers for Liver Injury in Zebrafish Larvae.

Liver plays a crucial role in detoxification processes and metabolism of xenobiotics, and therefore, it is a target organ of toxicity of different classes of chemicals. In this context, some key enzymes present in liver are considered to be good biochemical markers of hepatic damage and can have their activities determined via spectrophotometry. Aspartate and alanine aminotransferases, alkaline phosphatase, lactate dehydrogenase, and glutathione peroxidase are enzymes that have activities often changed in response to hepatotoxic compounds and can be accessed through the larval period of zebrafish (Danio rerio). In this chapter, we described methodologies for analyses of these five biomarkers in pooled zebrafish larvae through spectrophotometry.

Acid-base abnormalities and liver dysfunction.

In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the regulation of ABE is crucial because of its role in lactic acid metabolism, urea production and in protein homeostasis. The main acid-base imbalance that occurs in patients with liver cirrhosis is Respiratory Alkalosis (RAlk). Due to the fact that in these patients additional pathophysiological mechanisms that affect the ABE are present, other disorders may appear which compensate or enhance the primary disorder. Conventional ABE reading models fail to identify and assess the underlying disorders in patients with liver cirrhosis. This weakness of the classical models led to the creation of new physicochemical mathematical models that take into account all the known parameters that develop and affect the ABE. In addition to the RAlk, in patients with liver cirrhosis, metabolic alkalosis (due to hypoalbuminemia), hyponatremic metabolic acidosis, hyperchloremic metabolic acidosis, lactic acidosis and metabolic alkalosis due to urea metabolism are some of the pathophysiological mechanisms that affect the ABE.

Toxic Effect of Aflatoxins in Dogs Fed Contaminated Commercial Dry Feed: A Review.

Since its first patent (1897), commercial dry feed (CDF) for dogs has diversified its formulation to meet the nutritional needs of different breeds, age, or special conditions and establish a foundation for integration of these pets into urban lifestyles. The risk of aflatoxicosis in dogs has increased because the ingredients used to formulate CDF have also proliferated, making it difficult to ensure the quality required of each to achieve the safety of the entire CDF. This review contains a description of the fungi and aflatoxins detected in CDF and the ingredients commonly used for their formulation. The mechanisms of action and pathogenic effects of aflatoxins are outlined; as well as the clinical findings, and macroscopic and microscopic lesions found in aflatoxicosis in dogs. In addition, alternatives for diagnosis, treatment, and control of aflatoxins (AF) in CDF are analyzed, such as biomarkers of effect, improvement of blood coagulation, rate of elimination of AF, control of secondary infection, protection of gastric mucosa, reduction of oxidative stress, use of chemo-protectors, sequestrants, grain-free CDF, biocontrol, and maximum permitted limits, are also included.

Congenital Torsion of a Herniated Accessory Liver Lobe in a Lamb

Accessory liver lobe (ALL) is an extremely rare anomaly, which can potentially undergo torsion and ischemia. A case with a herniated and twisted ALL originating from the umbilical fissure in conjunction with liver proper and lung abnormalities in a 2-day-old lamb is presented. The primitive presentation of the case was umbilical hernia that underwent herniorrhaphy and expired because of multiple anomalies. ALL seems to be caused by extra-embryonic entrapment of a portion of the liver as a result of high intra-abdominal pressure.(AU)

Congenital Torsion of a Herniated Accessory Liver Lobe in a Lamb

Accessory liver lobe (ALL) is an extremely rare anomaly, which can potentially undergo torsion and ischemia. A case with a herniated and twisted ALL originating from the umbilical fissure in conjunction with liver proper and lung abnormalities in a 2-day-old lamb is presented. The primitive presentation of the case was umbilical hernia that underwent herniorrhaphy and expired because of multiple anomalies. ALL seems to be caused by extra-embryonic entrapment of a portion of the liver as a result of high intra-abdominal pressure.

Hepatopatología para gastroenterólogos y hepatólogos: segunda parte: terminología útil en la interpretación de los hallazgos histopatológicos / Hepatopathology for gastroenterologists and hepatologists: part two useful terminology in the interpretation of the histopathological findings

Hepatic diseases, histology, hepatology, diagnostic histology, hepatic cells

Hepatic diseases, histology, hepatology, diagnostic histology, hepatic cells

Intoxicação experimental por aflatoxina em bezerros / Experimental aflatoxin poisoning in calves

Foram realizados dois experimentos para determinar os efeitos tóxicos de diferentes doses de aflatoxinas em bezerros, considerando-se aspectos clínicos, produtivos e patológicos. ... No primeiro experimento, o ganho de peso dos bezerros recebendo AFB1 foi equivalente ao do grupo controle durante todo período experimental. ...Durante o período experimental, e três semanas após o término desse período, não foram observados sinais clínicos e alterações histopatológicas associadas ao consumo de aflatoxinas, em qualquer dos bezerros do grupo tratamento do primeiro experimento.... Níveis alterados da atividade sérica de FA e GGT foram observados em todos os bezerros do grupo tratamento durante grande parte do período experimental. Queda acentuada do nível da AS sérica foi observada na coleta do 49º dia do experimento no bezerro que recebia a maior dose de aflatoxina. Não foram observadas variações no hematócrito e na atividade sérica da AST, nem nos níveis séricos de proteína total, bilirrubina total e bilirrubina direta em qualquer dos bezerros desse experimento. Alterações histopatológicas nos bezerros intoxicados incluíram proliferação de ductos biliares, degeneração citoplasmática vacuolar consistente com acumulação hepatocelular de lipídios, fibrose periportal, ou em ponte, megalocitose, fibrose subendotelial das veias hepáticas terminais e edema. Achados de necropsia do bezerro recebendo a maior dose de AFB1 incluíram fígado levemente aumentado de tamanho, difusamente amarelo-claro e firme, discreta ascite, edema de mesentério e submucosa do abomaso. Os dados obtidos nesses experimentos permitem afirmar que doses de 500±100 ppb de AFB1 não causam alterações patológicas e produtivas em bezerros em condições experimentais, mas podem estar associadas à mínimas alterações bioquímicas, enquanto doses de 1.250, 2.500 e 5.000 ppb de aflatoxina B1 causam doença hepática crônica em bezerros em condições experimentais.(AU)

Two experiments were performed in order to determine the toxic effects of varying doses of aflatoxins in calves. Clinical, productive and pathologic aspects of affected calves were considered….During all the experimental period of the first experiment, the weight gain of the calves receiving AFB1 was equivalent to that of the control group.…During the whole experimental period and up to three weeks after the final of the experiment, no clinical signs or histopathological changes associated with the consumption of aflatoxins were observed in any of the calves of the first experiment….Increased activity of AF and GGT were observed in all the calves of the treated group during most part of the experimental period. A marked drop in the serum levels of SA was observed in the serum sampled on the 49º day of the experiment in the calf receiving. the largest dose of aflatoxin. No changes were observed regarding PCV, TP, total bilirubin, direct bilirubin and in the serum activity of AST in any of the calves of the second experiment. Histopathological changes in intoxicated calves included bile duct proliferation, cytoplasmic vacuolar hepatocelular degeneration consistent with hepatocelular deposit of lipids, periportal to bridging fibrosis, megalocytosis, subendothelial edema and fibrosis in terminal hepatic veins. Necropsy findings in the euthanatized calf which receive de largest doses of AFB1 included slight enlargement of the liver which was firm and diffusely light-yellow, mild ascites, and edema of the mesentery and of abomasal folds. Data stemmed from these two experiments allow to conclude that AFB1 doses of 500±100 in the ration do not cause pathologic changes or decrease in productivity in calves kept in experimental conditions, but can be associated to minimal serum biochemistry; while AFB1 doses of 1.250, 2.500 e 5.000 ppb in the ration cause chronic hepatic disease in calves in kept in experimental conditions.(AU)

Intoxicação experimental por aflatoxina em bezerros / Experimental aflatoxin poisoning in calves

Foram realizados dois experimentos para determinar os efeitos tóxicos de diferentes doses de aflatoxinas em bezerros, considerando-se aspectos clínicos, produtivos e patológicos. ... No primeiro experimento, o ganho de peso dos bezerros recebendo AFB1 foi equivalente ao do grupo controle durante todo período experimental. ...Durante o período experimental, e três semanas após o término desse período, não foram observados sinais clínicos e alterações histopatológicas associadas ao consumo de aflatoxinas, em qualquer dos bezerros do grupo tratamento do primeiro experimento.... Níveis alterados da atividade sérica de FA e GGT foram observados em todos os bezerros do grupo tratamento durante grande parte do período experimental. Queda acentuada do nível da AS sérica foi observada na coleta do 49º dia do experimento no bezerro que recebia a maior dose de aflatoxina. Não foram observadas variações no hematócrito e na atividade sérica da AST, nem nos níveis séricos de proteína total, bilirrubina total e bilirrubina direta em qualquer dos bezerros desse experimento. Alterações histopatológicas nos bezerros intoxicados incluíram proliferação de ductos biliares, degeneração citoplasmática vacuolar consistente com acumulação hepatocelular de lipídios, fibrose periportal, ou em ponte, megalocitose, fibrose subendotelial das veias hepáticas terminais e edema. Achados de necropsia do bezerro recebendo a maior dose de AFB1 incluíram fígado levemente aumentado de tamanho, difusamente amarelo-claro e firme, discreta ascite, edema de mesentério e submucosa do abomaso. Os dados obtidos nesses experimentos permitem afirmar que doses de 500±100 ppb de AFB1 não causam alterações patológicas e produtivas em bezerros em condições experimentais, mas podem estar associadas à mínimas alterações bioquímicas, enquanto doses de 1.250, 2.500 e 5.000 ppb de aflatoxina B1 causam doença hepática crônica em bezerros em condições experimentais.

Two experiments were performed in order to determine the toxic effects of varying doses of aflatoxins in calves. Clinical, productive and pathologic aspects of affected calves were considered….During all the experimental period of the first experiment, the weight gain of the calves receiving AFB1 was equivalent to that of the control group.…During the whole experimental period and up to three weeks after the final of the experiment, no clinical signs or histopathological changes associated with the consumption of aflatoxins were observed in any of the calves of the first experiment….Increased activity of AF and GGT were observed in all the calves of the treated group during most part of the experimental period. A marked drop in the serum levels of SA was observed in the serum sampled on the 49º day of the experiment in the calf receiving. the largest dose of aflatoxin. No changes were observed regarding PCV, TP, total bilirubin, direct bilirubin and in the serum activity of AST in any of the calves of the second experiment. Histopathological changes in intoxicated calves included bile duct proliferation, cytoplasmic vacuolar hepatocelular degeneration consistent with hepatocelular deposit of lipids, periportal to bridging fibrosis, megalocytosis, subendothelial edema and fibrosis in terminal hepatic veins. Necropsy findings in the euthanatized calf which receive de largest doses of AFB1 included slight enlargement of the liver which was firm and diffusely light-yellow, mild ascites, and edema of the mesentery and of abomasal folds. Data stemmed from these two experiments allow to conclude that AFB1 doses of 500±100 in the ration do not cause pathologic changes or decrease in productivity in calves kept in experimental conditions, but can be associated to minimal serum biochemistry; while AFB1 doses of 1.250, 2.500 e 5.000 ppb in the ration cause chronic hepatic disease in calves in kept in experimental conditions.

Surto de aflatoxicose em bezerros no Rio Grande do Sul / Outbreak of aflatoxicosis in calves in southern Brazil

Um surto de aflatoxicose crônica é relatado em bezerros de raça leiteira. Quarenta bezerros holandeses machos de quatro meses de idade e aproximadamente 100kg eram mantidos em gaiolas individuais de 1,5 x 1,5m e alimentados com uma ração constituída por feno de alfafa, milho quebrado e substituto de leite. Seis bezerros (15 por cento) morreram após apresentar uma doença caracterizada por mau desenvolvimento geral, diarreia, pelagem áspera, dor abdominal, tenesmo, prolapso de reto e bruxismo. Alguns bezerros "deitavam e rolavam" no chão da gaiola. A duração do curso clínico, segundo observado pelos proprietários, foi de 2-3 dias; muitos terneiros desse lote que não morreram permaneceram pouco desenvolvidos. Três bezerros foram necropsiados. Os achados de necropsia incluíam fígado firme e castanho-claro, marcados hidrotórax e ascite, e edema do mesentério, mesocólon e das dobras da mucosa do abomaso. Os principais achados histopatológicos estavam restritos ao fígado e consistiam de fibrose, moderada megalocitose, hiperplasia de ductos biliares e lesão veno-oclusiva. A procura por contaminação de Senecio spp. no feno de alfafa resultou negativa. A análise do milho do alimento dos bezerros por cromatografia de camada delgada revelou 5.136ppb de aflatoxina B1. O diagnóstico de aflatoxicose foi feito baseado nos sinais clínicos e patologia característicos, na ausência de Senecio spp. na alimentação dos terneiros e na presença de altos níveis de aflatoxina no milho da alimentação dos bezerros.(AU)

An outbreak of chronic aflatoxicosis is reported in dairy calves. Forty 4-month-old male Holstein calves of approximately 100kg were kept in individual cages of 1.5 x 1.5m and were fed a ration constituted by alfalfa hay, broken corn and milk substitute. Six calves (15 percent) died after presenting a disease characterized by general unthriftiness, diarrhea, rough hair coats, abdominal pain, prolapsed rectum, grinding of teeth, and lying down and rolling. The clinical course, as observed by the owners, was 2-3 days; however many calves in this lot that did not die, remained underdeveloped. Three calves were necropsied. Necropsy findings included firm, light tan livers and marked hydrothorax, ascites and edema of the mesentery, mesocolon and of the mucosal folds of the abomasum. Main histopathological changes were restricted to the liver and consisted of fibrosis, moderate megalocytosis, biliary duct hyperplasia and veno-occlusive disease. The search for Senecio spp. contamination in the alfalfa hay resulted negative. The analysis by thin layer chromatography of the corn fed to calves revealed 5,136 ppb of aflatoxin B1. A diagnosis of aflatoxicosis was made based on the characteristic clinical signs and pathology, on the absence of Senecio spp. in the food and on the presence of high levels of aflatoxin in the corn fed to the calves.(AU)

Surto de aflatoxicose em bezerros no Rio Grande do Sul / Outbreak of aflatoxicosis in calves in southern Brazil

Um surto de aflatoxicose crônica é relatado em bezerros de raça leiteira. Quarenta bezerros holandeses machos de quatro meses de idade e aproximadamente 100kg eram mantidos em gaiolas individuais de 1,5 x 1,5m e alimentados com uma ração constituída por feno de alfafa, milho quebrado e substituto de leite. Seis bezerros (15 por cento) morreram após apresentar uma doença caracterizada por mau desenvolvimento geral, diarreia, pelagem áspera, dor abdominal, tenesmo, prolapso de reto e bruxismo. Alguns bezerros "deitavam e rolavam" no chão da gaiola. A duração do curso clínico, segundo observado pelos proprietários, foi de 2-3 dias; muitos terneiros desse lote que não morreram permaneceram pouco desenvolvidos. Três bezerros foram necropsiados. Os achados de necropsia incluíam fígado firme e castanho-claro, marcados hidrotórax e ascite, e edema do mesentério, mesocólon e das dobras da mucosa do abomaso. Os principais achados histopatológicos estavam restritos ao fígado e consistiam de fibrose, moderada megalocitose, hiperplasia de ductos biliares e lesão veno-oclusiva. A procura por contaminação de Senecio spp. no feno de alfafa resultou negativa. A análise do milho do alimento dos bezerros por cromatografia de camada delgada revelou 5.136ppb de aflatoxina B1. O diagnóstico de aflatoxicose foi feito baseado nos sinais clínicos e patologia característicos, na ausência de Senecio spp. na alimentação dos terneiros e na presença de altos níveis de aflatoxina no milho da alimentação dos bezerros.

An outbreak of chronic aflatoxicosis is reported in dairy calves. Forty 4-month-old male Holstein calves of approximately 100kg were kept in individual cages of 1.5 x 1.5m and were fed a ration constituted by alfalfa hay, broken corn and milk substitute. Six calves (15 percent) died after presenting a disease characterized by general unthriftiness, diarrhea, rough hair coats, abdominal pain, prolapsed rectum, grinding of teeth, and lying down and rolling. The clinical course, as observed by the owners, was 2-3 days; however many calves in this lot that did not die, remained underdeveloped. Three calves were necropsied. Necropsy findings included firm, light tan livers and marked hydrothorax, ascites and edema of the mesentery, mesocolon and of the mucosal folds of the abomasum. Main histopathological changes were restricted to the liver and consisted of fibrosis, moderate megalocytosis, biliary duct hyperplasia and veno-occlusive disease. The search for Senecio spp. contamination in the alfalfa hay resulted negative. The analysis by thin layer chromatography of the corn fed to calves revealed 5,136 ppb of aflatoxin B1. A diagnosis of aflatoxicosis was made based on the characteristic clinical signs and pathology, on the absence of Senecio spp. in the food and on the presence of high levels of aflatoxin in the corn fed to the calves.

Research on bilirrubine, urobilinogen and rate of serum bilirrubin in normal dogs and with hepatic diseases / Pesquisa de pigmentos biliares e urobilinogênio urinários e nível de bilirrubinas séricas em cães normais e com hepatopatias

An attempt was made at establishing a relationship between the presence of urinary liver pigments and/or urobilinogen and the rate of seric bilirrubine, in cases of hepatic diseases. The conclusion was that the presence of liver pigments, associated or not with urobilinogen in the urine indicates, hepatic involvement.

Procurou-se relacionar a presença de pigmentos biliares e/ou urobilinogênio urinários, com a taxa de bilirrubina sérica em casos de hepatopatias, observando-se que a presença de pigmentos biliares associadas ou não à presença de urobilinogênio na urina, indica de modo geral comprometimento hepático.

Research on bilirrubine, urobilinogen and rate of serum bilirrubin in normal dogs and with hepatic diseases / Pesquisa de pigmentos biliares e urobilinogênio urinários e nível de bilirrubinas séricas em cães normais e com hepatopatias

An attempt was made at establishing a relationship between the presence of urinary liver pigments and/or urobilinogen and the rate of seric bilirrubine, in cases of hepatic diseases. The conclusion was that the presence of liver pigments, associated or not with urobilinogen in the urine indicates, hepatic involvement.

Procurou-se relacionar a presença de pigmentos biliares e/ou urobilinogênio urinários, com a taxa de bilirrubina sérica em casos de hepatopatias, observando-se que a presença de pigmentos biliares associadas ou não à presença de urobilinogênio na urina, indica de modo geral comprometimento hepático.