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Aim: To evaluate the association between elevated serum transaminase levels and insulin resistance (IR) in a population of healthy individuals. Methods: We define IR with a cut-off point of homeostatic model assessment (HOMA-IR) ≥ 3.8. For aspartate aminotransferase (AST), we consider elevated values >30 U/L in women and values >36 U/L in men. For alanine aminotransferase (ALT), we consider elevated values >30 U/L in women and values >40 U/L in men. We performed a crude and adjusted generalized linear model from Poisson family with robust variance, in order to evaluate the association between elevated serum transaminase levels and IR. The associations were presented as prevalence ratio (PR) with their respective 95% confidence intervals (95% CI). Results: We included 261 participants in the study. The median age was 39 years (31–45) and 23.7% of the participants were men. The prevalence of elevated serum transaminase for AST and ALT were, 13.8% and 26.1%, respectively. The prevalence of IR was 34.1%. In the crude analysis we found statistical significance between elevated AST and ALT with IR (PR = 3.18; 95% CI: 2.33–4.34 and PR = 2.44; 95% CI: 1.88–3.30; respectively). However, in the multivariate analysis, the association only remained statistically significance with ALT, but lost its significance with AST, PR = 1.90; CI 95%: 1.31–2.77 and a PR = 1.23; CI 95%: 0.93–1.61; respectively. Conclusion: Elevated serum levels of ALT were associated with insulin resistance. ALT could be used in clinical practice as an additional tool to assess IR in apparently healthy people. / Dirección de Gestión de la Investigación, Universidad de Antofagasta / Revisión por pares

In malting barley, rapid germination is desirable and linked to end use quality. Modern malting varieties have been bred for low seed dormancy leading to issues with pre-harvest sprouting in wetter growing regions. To maintain malting capacity while minimizing germination on the maternal plant requires in-depth understanding of the genetic regulation of dormancy in malting barley. Currently, the major effect QTLs SD1 and SD2 have been shown to influence dormancy across multiple populations of barley, though the physiological mechanisms involved remain unclear. To search for novel genetic regions that influence primary dormancy, three mapping populations were assessed including two Canadian biparental populations (Synch and Legci) as well as a diversity panel sourced from multiple locations worldwide (ICARDA AM-14). The SD2 locus had a major effect in the Synch population while the SD1 locus had a major effect in the Legci population and neither SD1 nor SD2 were linked to dormancy in the diversity panel. Instead, 14 additional marker trait associations were identified in AM-14 suggesting that investigating a broader range of genetic regulation of dormancy outside of North American varieties may provide solutions to regulate this trait. Additional testing on SD1 revealed that variation at this locus did not affect ABA sensitivity during germination or GA or ABA-regulated gene expression during grain fill. Indeed, lines containing the non-dormant SD1 allele germinate at a similar rate as the dormant SD1 seeds when the glumella was removed from the embryo. This indicated that the effect of the alanine aminotransferase gene underlying the SD1 allele is dependent on physical restriction on the embryo or the hypoxic effects produced by the glumella. Imposing a hypoxic (5% oxygen) environment on exposed embryos revealed an association between non-dormancy at SD1 and reduced sensitivity to the suppressive effects of hypoxia on germination. This suggests that alanine aminotransferase regulates dormancy release during barley germination at least in part through regulation of the seed’s response to hypoxia.

As nitrogen (N) is a critical nutrient for plant growth, the development of synthetic N fertilisers dramatically changed agricultural production in the twentieth century. Improvement in N use efficiency (NUE) has been a focus of breeding for grain crop species, since protein is an important component of the harvested product. The study of NUE in sugarcane has lagged behind grain crops, mainly because N is not a component of sucrose, the primary product of the traditional sugarcane industry. Recently, improvement in NUE has become a focus of sugarcane breeding, due largely to environmental concerns regarding pollution from high N fertilisation, and the increasing cost of N fertilisers. This thesis aimed to gain an initial understanding of the genetic basis for variability in NUE in sugarcane. This was achieved through: (i) the screening of 168 sugarcane genotypes under limiting and non-limiting N supply in two glasshouse experiments; (ii) the mapping of marker-trait associations (MTA) for biomass and physiological traits under limiting and non-limiting N supply in a sugarcane mapping population; (iii) the analysis of expression of candidate genes encoding enzymes involved in the central processes of N assimilation and remobilisation in plants; and (iv) the mapping of candidate genes in a sugarcane genetic map. Genetic variation was identified for growth traits as well as physiological traits including %N, internal NUE (iNUE, g dry weight g-1 N) and leaf glutamine synthetase (GS) activity in a sugarcane mapping population. These traits were also analysed for linkage with genetic markers. Genetic variation in the screened genotypes was higher under limiting N supply, a finding that was reflected by the fact that marker-trait associations (MTA) for increases in iNUE were not identified under non-limiting N supply in the commercial parent of the mapping population. Contrary to findings in grain crop species, there was no link between GS activity and other traits, either through phenotypic correlations or co-location of MTA. The expression of candidate genes encoding GS, nitrate reductase (NR) and alanine amintotransferase (AlaAT) was quantified with Sequenom™ MassARRAY technology. Plants were grown under growth-limiting N supply, non-limiting N supply, or a N-pulse treatment, which consisted of growth-limiting N supply followed by non-limiting N supply 24 hours prior to sampling. Two genes, scAlaAT.d and scGS1.a, encoding AlaAT and GS respectively, were identified as non-responsive to changes in N supply, whereas scAlaAT.a, scGS1.b and scGS1.c had significantly (p<0.05) increased expression under a N-pulse, indicating an important role for these genes in the response of sugarcane to a sudden increase in N availability. The location of candidate genes associated with variation in NUE in a sugarcane genetic map were sought through restriction fragment length polymorphism (RFLP) markers. Twenty-two probes were screened, of which two generated single-dose markers, allowing the mapping of a single allele of scAspAT, encoding aspartate aminotransferase, and two alleles of scGS2, encoding plastidic GS. Because of the economic and environmental consequences of inefficient N fertiliser application, the development of sugarcane cultivars with improved NUE is essential. Since variation for NUE exists, especially in unimproved sugarcane varieties, this may be achieved through traditional breeding methods by screening existing breeding populations under limiting N supply. Additionally, an improved understanding of the genetic basis of variation for NUE in sugarcane should be pursued by further analysis of candidate gene response to changing N availability by screening widely varying cane species for differences in gene expression, enzyme activity and metabolite profiles. The further addition of candidate gene locations to sugarcane genetic maps will aid both future marker-assisted selection in breeding, and a fundamental understanding of genetic control of NUE variation. Through the development of sugarcane cultivars with improved NUE and an enhanced knowledge of the genetic control underpinning sugarcane N physiology, concerns regarding high N fertiliser applications may be mitigated and sustainability ensured.

Objetivo: Evaluar la asociación entre los niveles elevados de transaminasemia y resistencia a la insulina en una población de individuos sin alteraciones laboratoriales previas de glicemia, insulinemia, ni tiroideos. Métodos: Realizamos un modelo lineal generalizado crudo y ajustado de la familia Poisson con una varianza robusta, para evaluar la asociación entre los niveles elevados de transaminasemia y resistencia a la insulina. Las asociaciones se presentaron como razón de prevalencia (RP) con sus respectivos intervalos de confianza al 95%. Resultados: Se incluyeron 261 participantes. La mediana de edad fue de 39 años (31-45) y el 23,7% de los participantes eran hombres. La prevalencia de transaminasas séricas elevadas para TGO y TGP fue de 13.8% y 26.1%, respectivamente. La prevalencia de resistencia a la insulina fue del 34,1%. En el análisis en bruto encontramos significancia estadística entre TGP y TGO elevados y resistencia a la insulina (RP = 3,18; IC del 95%: 2,33-4,34 y RP = 2,44; IC del 95%: 1,88 a 3,30; respectivamente). Sin embargo, en el análisis multivariado ajustado, la asociación entre el nivel elevado de transaminasas séricas y la resistencia a la insulina permaneció estadísticamente significativa con TGP, pero se perdió con TGO; un PR = 1.90; CI95%: 1.31-2.77 y un PR = 1.23; CI95%: 0,93-1,61; respectivamente. Conclusión: niveles séricos elevados de TGP se asociaron con resistencia a la insulina. TGP podría usarse en la práctica clínica como una herramienta adicional para evaluar la resistencia a la insulina en personas sin alteraciones laboratoriales previas de glicemia, insulinemia, ni tiroideos. / Aim: To evaluate the association between elevated serum transaminase levels and insulin resistance in a population of individuals without alterations in their laboratorial values of glycemia, insulinemia and thyroid panel. Methods: We performed a crude and adjusted generalized linear model of the Poisson family with robust variance, in order to evaluate the association between elevated serum transaminase levels and insulin resistance. The associations were presented as prevalence ratio (PR) with their respective 95% confidence intervals (95% CI). Results: We included 261 participants in the study. The median age was 39 years (31-45) and 23,7% of the participants were men. The prevalence of elevated serum transaminase for TGO and TGP were, 13.8% and 26.1%, respectively. The prevalence of insulin resistance was 34,1%. In the crude analysis we found statistical significance between elevated TGP and TGO and insulin resistance (PR=3,18; 95% CI: 2,33-4,34 and PR=2.44; 95% CI: 1.88-3.30; respectively). However, in the multivariate analysis adjusted for age, sex, body mass index and thyroid hormones, the association between the elevated serum transaminase level and insulin resistance remained statistically significance with TGP, but lost its significance with TGO; a PR = 1.90; CI95%: 1.31-2.77 and a PR = 1.23; CI95%: 0.93-1.61; respectively. Conclusion: Elevated serum levels of TGP were associated with insulin resistance. TGP could be used in clinical practice as an additional tool to assess insulin resistance in people without laboratorial alterations in glycemia, insulinemia and thyroid panel. / Tesis

Los peces carnívoros presentan baja capacidad para utilizar carbohidratos provenientes de la dieta y controlar los niveles de glucosa en sangre. En comparación con los mamíferos, estos animales tras la ingesta de glucosa o de dietas con alto contenido en carbohidratos, muestran una hiperglucemia mas prolongada. La alanina aminotransferasa (ALT) constituye un nexo de interacción entre el metabolismo de aminoácidos y el de carbohidratos al catalizar la reacción de la transaminación reversible entre L-alanina y 2-oxoglutarato para formar piruvato y L-glutamato. Estudios previos de nuestro grupo indicaron la presencia de tres isoformas ALT en dorada (Sparus aurata): las isoenzimas citosólicas cALT1 y cALT2 y una isoforma mitocondrial, mALT. En hígado de dorada, la expresión de cALT2 incrementa en situación de gluconeogénesis mientras que cALT1 predomina durante el período postprandial para la utilización de los nutrientes de la dieta. El objetivo general del presente estudio es comprender a nivel molecular los efectos metabólicos derivados de la inhibición de ALT en peces para ayudar a establecer nuevas aplicaciones biotecnológicas orientadas a mejorar la utilización de los nutrientes de la dieta. Así, en acuicultura, identificar los efectos metabólicos asociados a la modulación de la actividad ALT constituye un punto de interés para conocer si es posible efectuar una sustitución parcial de las proteínas de la dieta por carbohidratos u otros nutrientes, a fin de reducir el coste de la producción en acuicultura y disminuir la eutrofización de las aguas del entorno. Nuestros estudios muestran que la inyección intraperitoneal de doradas con nanopartículas del complejo pCpG-siRNA-quitosán resultó adecuada para promover la expresión de un siRNA para bloquear la expresión de cALT1 en hígado de Sparus aurata. La inyección intraperitoneal de nanopartículas de pCpGsi1sh1-quitosán promovió la silenciación de cALT1 a nivel de mRNA y actividad enzimática en hígado de dorada. Por otra parte, hemos analizado la inhibición postranscripcional de la actividad ALT in vivo e in vitro con el compuesto aminooxiacetato (AOA) y analizado los cambios promovidos en metabolitos y enzimas clave en el metabolismo intermediario de carbohidratos y proteínas en hígado de Sparus aurata, tras la ingesta del AOA con dietas de diferente composición. In vitro, el AOA ejerce una inhibición dependiente de dosis sobre la actividad ALT hepática citosólica y mitocondrial. In vivo, el AOA se comportó como inhibidor de la actividad ALT citosólica hepática, pero no de la mitocondrial. Una exposición a largo plazo a AOA promovió un aumento de la actividad piruvato quinasa en el hígado de dorada, independientemente de la composición de la dieta suministrada a los peces. Los estudios de 1H-RMN mostraron que la inclusión de AOA en la dieta promueve una disminución en los niveles hepáticos de alanina, glutamato y glucógeno. Adicionalmente, los análisis de 2H-RMN indicaron una tasa de renovación más alta de alanina en el hígado de los peces alimentados con una dieta con un contenido alto en carbohidratos y bajo en proteínas y que el AOA disminuye el enriquecimiento de alanina en 2H independientemente de la composición de la dieta. Los estudios derivados de esta tesis indican que la inhibición dependiente de AOA de la actividad de la ALT citosólica podría contribuir a aumentar el uso de nutrientes por carbohidratos de la dieta de Sparus aurata. / Carnivorous fish have low ability to utilize dietary carbohydrates and controlling blood glucose levels. Compared with mammals, these animals after ingestion of glucose or diets high in carbohydrates show a more prolonged hyperglycemia. Alanine aminotransferase (ALT) links carbohydrate and amino acid metabolism through catalysing the reversible transamination between L-alanine and 2-oxoglutarate to form pyruvate and L-glutamate. Previous studies from our group indicated the presence of three isoforms ALT bream (Sparus aurata): cALT1 cytosolic isoenzymes and cALT2 and a mitochondrial isoform, mALT. In the liver os Sparus aurata cALT2 expression increases gluconeogenesis situation prevails while cALT1 during the postprandial period for the utilization of dietary nutrients. The overall objective of this study is to understand at a molecular level the resulting metabolic effects from the inhibition of ALT in fish to help establish new biotechnological applications aimed to improve the use of dietary nutrients. Thus in aquaculture, identifying metabolic effects associated with ALT activity modulation is a point of interest to know if it is possible to perform a partial replacement of dietary proteins by carbohydrate or other nutrients, to reduce the cost of Aquaculture production and reduce eutrophication of the environment. Our studies show that intraperitoneal injection of a chitosan-pCpG-siRNA nanoparticles complex to Gilthead seabream proved to be suitable for the expression of a siRNA to silence the expression of liver cALT1 in Sparus aurata. Intraperitoneal injection of pCpGsi1sh1-chitosan nanoparticles complex promoted cALT1 silencing at the mRNA level and a decrease of liver enzyme activity of Gilthead seabream. In the present study amino-oxyacetate (AOA) was used to evaluate its effect on liver ALT activity of the carnivorous fish Sparus aurata. Moreover, the derived metabolic effects on metabolites and other key enzymes of glycolysis, gluconeogenesis and the pentose phosphate pathway were also studied. A dose-effect-dependent inhibition of AOA on hepatic cytosolic and mitochondrial ALT activity was observed in vitro. In vivo, AOA behaved as an inhibitor of hepatic cytosolic ALT activity. A long-term exposure to AOA increased pyruvate kinase activity in the liver irrespective of the composition of the diet supplied to fish. 1H NMR studies showed that inclusion of AOA to the diet decreased the hepatic levels of alanine, glutamate and glycogen. Moreover, 2H NMR analysis indicated a higher renewal rate for alanine in the liver of fish fed with a high-carbohydrate/low-protein diet, while AOA decreased alanine 2H-enrichment irrespective of the diet. The present study indicates that AOA-dependent inhibition of the cytosolic ALT activity could help to increase the use of dietary carbohydrate nutrients by the Sparus aurata fish.

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / Mercury is an environmental contaminant, and may accumulate in living organisms causing several damage. Studies have shown that this metal causes several physiological and biochemical alterations in young rats which are prevented by zinc. Thus, this work investigated the in vivo and in vitro effects of HgCl2 and ZnCl2 on alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and glucose 6-phosphatase (G6Pase) activities from liver and kidney of young rats to verify if the physiological and biochemical alterations induced by mercury, and prevented by zinc, are related to hepatic and renal metabolism. Glycemia and tissue glycogen levels (liver, kidney and muscle) were also monitored. Wistar rats were treated (s.c.) with saline or ZnCl2 (27 mg/kg/day) and with saline or HgCl2 (5.0 mg/kg/day) from 3rd to 7th and 8th to 12th days of age, respectively. Pups were sacrificed 24h after the last dose and samples were collected (blood, liver, kidney and muscle). For in vitro experimentation, the samples were collected similarly, with rats of 10 to 13 days old. Regarding in vivo experiments, the mercury treated rats presented an increase around 6 folds of the hepatic ALT activity, without alteration of renal ALT and hepatic LDH activities. Still, the mercury exposure significantly increases in 75% the G6Pase activity. The other parameters, glucose and glycogen, were not altered. The pre-exposure to zinc prevented totally the increase of liver ALT activity and partly the increase of hepatic G6Pase activity induced by mercury. In vitro results revealed that the serum and liver ALT and liver and kidney G6Pase activities were inhibited by mercury. The inhibitory effect may be related to chemical modification of sulfhydryl group of cysteine, since the mercury has great affinity for these groups, which contributes to its toxicity. Zinc inhibited liver and serum ALT activities in concentration of 100 μM. These results show that mercury induces distinct alterations in these enzymes when tested in vivo or in vitro, as well as when different sources of enzyme were used, hepatic and renal. The increased hepatic ALT and G6Pase activities suggest that animals exposed to mercury have an increased gluconeogenic activity in this tissue. Zinc prevents the in vivo effects of mercury on metabolic changes, confirming its important preventive role. / O mercúrio é um elemento tóxico, podendo acumular-se em organismos vivos causando-lhes vários danos. Estudos têm demonstrado que esse metal é capaz de causar várias alterações fisiológicas e bioquímicas em ratos jovens, as quais são prevenidas pela pré-exposição ao zinco. Assim, este trabalho investigou os efeitos in vivo e in vitro do HgCl2 e ZnCl2 sobre as atividades das enzimas alanina aminotransferase (ALT), lactato desidrogenase (LDH) e glicose 6-fosfatase (G6Pase) de fígado e rim de ratos jovens para verificar se as alterações fisiológicas e bioquímicas induzidas pelo mercúrio e impedidas pelo zinco, estão relacionados ao metabolismo hepático e renal. Os níveis glicêmicos e do glicogênio tecidual (fígado, rim e músculo) também foram monitorados. Ratos Wistar com três dias de idade foram tratados (s.c.) com salina ou ZnCl2 (27 mg/kg/dia) durante cinco dias consecutivos (do 3 o ao 7 o dia de idade) e com salina ou HgCl2 (5 mg/kg/dia) por mais cinco dias (do 8 o ao 12 o dia de idade). Os animais foram sacrificados 24 horas após a última dose e as amostras foram coletadas (sangue, fígado, rim e músculo). Para realização dos experimentos in vitro, amostras foram coletadas de maneira similar, com ratos de 10-13 dias de idade. Com relação aos experimentos in vivo, os ratos tratados com mercúrio apresentaram um aumento da atividade da ALT hepática de aproximadamente seis vezes, sem alteração da atividade da ALT renal e LDH hepática. Ainda, a exposição ao mercúrio aumentou significativamente a atividade da G6Pase em 75%. Os outros dois parâmetros, glicose e glicogênio, não foram alterados. A pré-exposição ao zinco preveniu a alteração da atividade da ALT e parcialmente a alteração da atividade da G6Pase hepática induzida pelo mercúrio. Os resultados in vitro demonstraram que as enzimas ALT e LDH sérica e hepática e G6Pase hepática e renal foram inibidas por mercúrio. O efeito inibitório pode estar relacionado às modificações químicas de grupos sulfidrílicos da cisteína, uma vez que o mercúrio tem grande afinidade por esses grupos, o que contribui para a sua toxicidade. O zinco inibiu a atividade da ALT hepática e sérica na concentração de 100 μM. Estes resultados mostram que o mercúrio induziu alterações distintas sobre essas enzimas quando testado in vivo e in vitro, bem como quando testado em enzimas provenientes de diferentes fontes, hepática e renal. O aumento da atividade das enzimas ALT e G6Pase de fígado sugerem que os animais expostos ao mercúrio apresentam um aumento da atividade gliconeogênica. O zinco previne os efeitos in vivo do mercúrio sobre as alterações metabólicas, confirmando seu papel protetor.

Submitted by Luciana Ferreira (lucgeral@gmail.com) on 2014-11-07T10:55:53Z No. of bitstreams: 2 Dissertação - Mirian de Sylvio - 2009.pdf: 865608 bytes, checksum: bba24a89ef1938c31376520a3eff1e60 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) / Approved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2014-11-07T11:29:38Z (GMT) No. of bitstreams: 2 Dissertação - Mirian de Sylvio - 2009.pdf: 865608 bytes, checksum: bba24a89ef1938c31376520a3eff1e60 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) / Made available in DSpace on 2014-11-07T11:29:38Z (GMT). No. of bitstreams: 2 Dissertação - Mirian de Sylvio - 2009.pdf: 865608 bytes, checksum: bba24a89ef1938c31376520a3eff1e60 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) Previous issue date: 2009-12-15 / Infection with Toxoplasma gondii occurs throughout the globe, with a prevalence of up to 90% in the population. The physiological changes caused by this parasite are well studied in immunocompromised individuals and in cases of congenital transmission. In immunocompetent individuals the infection is usually asymptomatic and little explored by researchers. Experimental studies follow the pattern of human studies, and there fow mention about the biochemical changes (liver and kidney metabolisms) in the host infected by T. gondii. This study aimed the quantification of hepatic and kidney alterations caused by acute infections by T. gondii (non cystogenic strain – RH) and by chronic infections (cystogenic strain – ME-49). The control group was formed by mice without infection, only submitted to saline stress. Several enzymes were measured in serum and peritoneal exudate of mice infected and control such as: aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutamyltransferase (GGT), alkaline phosphatase (ALP), urea, creatinine and lactate dehydrogenase, using an automated methodology. AST and ALT presented a significative difference in the serum of mice infected with RH strain when compared to controls indicating a destruction of liver cells. The peritoneal exudates did not present significative changes in relation to controls nor did the urea and creatinine levels. The séric lactate dehydrogenase showed gradual changes in all days of the infection in mice peritoneal exudates as early as this change was evident only in the fifth day of infection. All samples of the group infected with ME-49 strain showed changes in serum and peritoneal exudate during all days of analysis. Only ALT peritoneal exudates showed no change during all days of analysis. An increase in urea at all doses was observed, however, creatinine showed a change only within 120 days of infection. The LDH was altered in the serum in all days of analysis. In conclusion, the T. gondii infection may cause hepatic and kidney injuries either when caused by non-cystogenic as by cystogenic strains of the parasite. / A infecção pelo Toxoplasma gondii ocorre em todo o mundo, com prevalência de até 90% na população conforme seus hábitos culturais e condições socioeconômicas. As alterações fisiopatológicas provocadas por este parasito são muito estudadas nos indivíduos imunocomprometidos, nos casos de transmissão congênita, e nos indivíduos imunocompetentes a infecção é, geralmente, assintomática e pouco explorada pelos pesquisadores. Experimentalmente, os estudos seguem o padrão dos estudos humanos, e há pouca referência sobre as alterações bioquímicas (hepáticas e renais) no hospedeiro infectado pelo T. gondii. Este trabalho objetivou avaliar as alterações hepáticas e renais causadas por esse parasito em camundongos na fase aguda, usando a cepa não cistogênica (RH), e na fase crônica, com a cepa cistogênica (ME-49), tendo como controles camundongos sem infecção, somente submetidos ao estresse de inoculação com salina. Foram dosadas no soro e no exsudato peritoneal dos camundongos infectados e controles os níveis das enzimas Aspartato aminotransferase (AST), Alanina aminotransferase (ALT), Gamaglutamiltransferase (GGT), Fosfatase alcalina (FAL), desidrogenase lática (DHL) e dos seguintes compostos: uréia e creatinina, por metodologia automatizada. As enzimas AST e ALT apresentaram diferença significativa no soro de camundongos infectados com cepa RH, demonstraram alterações em relação aos controles indicando uma destruição das células hepáticas. No exsudato peritoneal não foram demonstradas alterações em relação aos controles. A uréia e creatinina dosadas não demonstraram alteração significativa. A enzima lactato desidrogenase sérica apresentou alterações gradativas em todos os dias de infecção do camundongo no soro, já no exsudato peritoneal essa alteração foi evidenciada somente no quinto dia da infecção, mostrando que com o aumento de parasitos e a destruição celular causada por esse, essa enzima presente em várias células é responsável por demonstrar aumentos consideráveis. Todas as amostras de soro analisadas do grupo infectado com a cepa ME-49 demonstraram alterações durante todo período de acompanhamento. Enquanto que no exsudato peritoneal não mostrou nenhuma alteração durante todo período analisado. Houve aumento crescente na uréia em todos os dias de analises, porém, a creatinina não apresentou nenhuma alteração. A LDH mostrou-se alterada no soro em todos os dias de analisado. Conclui-se que a infecção pelo T. gondii pode provocar alterações hepáticas e renais ao longo do curso de infecção, tanto em infecções com cepa cistogênica quanto com cepa não cistogênica.