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RESUMOForam utilizados 23 touros da raça Nelore entre os 10 e 20 meses de idade, para caracterizar o desenvolvimento puberal. Os animais foram criados em condições extensivas com alimentação em pasto e suplementação mineral. A cada duas ou quatro semanas foram realizadas colheitas de dados que incluíram medidas de peso corporal, circunferência torácica, comprimento e largura testicular e circunferência escrotal. Foram, também, colhidos ejaculados pela eletroejaculação e avaliados os aspectos físicos e morfológicos. No momento da colheita de sêmen foram aferidas as porcentagens de desprendimento entre pênis e prepúcio e determinadas as idades médias ao desprendimento total (IDPPRE). Foram determinadas as idades médias ao aparecimento dos primeiros espermatozóides (ISEM1) e dos primeiros espermatozóides móveis (ISEM2) no ejaculado, e a puberdade seminal (IDPUB). Estabeleceram-se os índices de capacidade andrológica por pontos (ICAP). Os touros Nelore apresentaram idades médias ISEM1, ISEM2 e IDPUB de 13,1±2,2, 13,6±2,3 e 14,8±1,8 meses, respectivamente, e IDPPRE de 18,1±1,9. Aos 16 meses de idade, o grupo apresentou 91,4%, 82,6% e 73,9% dos animais com ISEM1, ISEM2 e IDPUB manifestada, respectivamente. Observou-se correlação positiva entre idade dos touros e as características de crescimento corporal, testicular, aspectos físicos dos ejaculados e correlação negativa entre a idade dos touros e os defeitos espermáticos. Observou-se correlação negativa entre a idade dos touros e a pontuação para circunferência escrotal no ICAP à puberdade (-0,77; P<0,001). Touros da raça Nelore, criados a pastos, manifestaram a puberdade precocemente antes dos 15 meses de idade. Houve um período de 51 dias desde o aparecimento dos espermatozóides no ejaculado, até a puberdade seminal. A puberdade foi mais precoce nos touros jovens com maiores testículos.Palavras-chave: bovino, Nelore, puberdade, testículo, sêmen, circunferência escrotal ABSTRACT

The correlation between apoptosis and early bovine embryonic loss is still not fully elucidated. In the present study, the relationship between the arrest of bovine embryos at the different stages of development and apoptosis was evaluated. We used embryos 7 days after in vitro maturation and fertilization, and morphologic and biochemical apoptotic analyses were performed by using a phase contrast microscope and by the terminal transferase dUTP nick end-labelling respectively. For the statistic, the apoptotic cell ratio (ACR) was determined as the percentage of apoptotic cells per embryo. To evaluate the relation between ACR and fragmentation pattern, embryos were divided into five groups, groups I-V. To assess the relation between ACR and cytoplasmatic fragmentation, embryos were divided into three groups, according to the fragmentation percentage (<5%; 5-15% and >15%). Of the total 139 embryos included, 65 arrested at 2-8 cells; 14 arrested at 9-16 cells; 18 compacted morula and 42 were non-arrested blastocysts. The average number of embryonic fragmentation at different stages of the development, 2-8 cells, 9-16 cells, compacted morula and blastocyst, was 16.0 +/- 1.5, 28.7 +/- 4.4, 4.4 +/- 2.4 and 1 +/- 0.3 respectively. The embryos at the stage of arrested 9-16 cells and compacted morula had higher ACR than those at the blastocyst stage, excluding the stage of 2-8 cells (the genome is not yet active). The correlation detected between embryonic development and ACR was 0.92 (p < 0.01). It was observed that embryos possessing high fragmentation showed the higher ACR value (r = 0.98, p < 0.05). Comparing the results between fragmentation percentage and ACR, it was observed that the embryos with higher percentage of fragmentation corresponded to higher ACR (r = 0.97, p < 0.01). These results clearly demonstrated that bovine embryonic arrest at different stages of development is correlated with the apoptotic mechanisms.

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Antioxidants are compounds that protect cells against the damaging effects of reactive oxygen species (ROS) such as singlet oxygen, superoxide, peroxyl radicals, hydroxyl radicals and peroxynitrite. Oxidative damage occurs to cells in vivo and in vitro from exposure to free radicals generated by exogenous agents (e.g., radiation, chemicals, hyperoxia) and endogenous processes such as normal cellular metabolism. An imbalance between antioxidants and ROS results in oxidative stress, leading to cellular damage. Oxidative stress (OS) has been linked to cancer, ageing, atherosclerosis, ischemic injury, inflammation, and neurodegenerative diseases. Under extreme oxidative conditions, or if the antioxidant protective mechanisms of cells are compromised, cellular injury and death may occur. Early mammalian embryos are susceptible to damage from reactive oxygen species, and they increase the production of oxygen free radicals when cultured in vitro. ROS generation results from mitochondria´s oxidative phosphorylation. The electrons will leak from the inner mitochondrial membranes, being transferred by the oxygen molecule, resulting in an unpaired electron in the orbit. This leaking results in the generation of the superoxide molecules. ROS can also be generated by the cytoplasmic NADPH-oxidase, cytochrome p450 enzymes and the xanthine oxidoreductase enzymes. The excess of OS can have negative effects on the cellular environment and can result in impaired cellular growth in the embryo or apoptosis resulting in embryo fragmentation. Similarly to what happens in females, oxidative energy production in males is inevitably associated with the generation of ROS excessive concentrations of which can lead to cellular pathology. It has been established that ROS can function as signaling molecules and evidence is emerging that sperm may generate low and controlled concentrations of ROS, specifically O 2-H 2 O 2 , as well as other species such as nitric oxide (NO), which, in his turn, act to mediate the processes of capacitation, hyperactivation and acrosome reaction crucial to the acquisition of fertilizing ability. In the present review the most important antioxidants and their mechanisms of action related to animal reproduction, are discussed.

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In comparison with white patients, black patients are two to three times more likely to be hospitalized for chronic pancreatitis than alcoholic cirrhosis. This highly significant (p < 0.001) difference was observed in both men and women: in three different hospitals, and in two different countries. The explanation is unknown, but could be related to racial differences in diet, type or quantity of alcohol consumption, smoking, or ability to detoxify substances harmful to the liver or pancreas.

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