S-adenosylmethionine and methylthioadenosine are antiapoptotic in cultured rat hepatocytes but proapoptotic in human hepatoma cells

S-adenosylmethionine (AdoMet) is an essential compound in cellular transmethylation reactions and a precursor of polyamine and glutathione synthesis in the liver. In liver injury, the synthesis of AdoMet is impaired and its availability limited. AdoMet administration attenuates experimental liver damage, improves survival of alcoholic patients with cirrhosis, and prevents experimental hepatocarcinogenesis. Apoptosis contributes to different liver injuries, many of which are protected by AdoMet. The mechanism of AdoMet's hepatoprotective and chemopreventive effects are largely unknown. The effect of AdoMet on okadaic acid (OA)-induced apoptosis was evaluated using primary cultures of rat hepatocytes and human hepatoma cell lines. AdoMet protected rat hepatocytes from OA-induced apoptosis dose dependently. It attenuated mitochondrial cytochrome c release, caspase 3 activation, and poly(ADP-ribose) polymerase cleavage. These effects were independent from AdoMet-dependent glutathione synthesis, and mimicked by 5'-methylthioadenosine (MTA), which is derived from AdoMet. Interestingly, AdoMet and MTA did not protect HuH7 cells from OA-induced apoptosis; conversely both compounds behaved as proapoptotic agents. AdoMet's proapoptotic effect was dose dependent and observed also in HepG2 cells. In conclusion, AdoMet exerts opposing effects on apoptosis in normal versus transformed hepatocytes that could be mediated through its conversion to MTA. These effects may participate in the hepatoprotective and chemopreventive properties of this safe and well-tolerated drug

TRIB3 suppresses tumorigenesis by controlling mTORC2/AKT/FOXO signaling.

In a recent article, we found that Tribbles pseudokinase 3 (TRIB3) plays a tumor suppressor role and that this effect relies on the dysregulation of the phosphorylation of v-akt murine thymoma viral oncogene homolog (AKT) by the mammalian target of rapamycin complex 2 (mTORC2 complex), and the subsequent hyperphosphorylation and inactivation of the transcription factor Forkhead box O3 (FOXO3)

Teores de colesterol e oxidação lipídica em hambúrguer bovino com adição de linhaça dourada e derivados

O objetivo deste trabalho foi avaliar o efeito da adição de linhaça‑dourada e derivados sobre os teores de colesterol e a oxidação lipídica em hambúrguer bovino. Foram elaborados hambúrgueres com 5,0% de óleo, ou farinha, ou sementes de linhaça‑dourada, além de uma formulação‑controle (sem adição de linhaça ou derivados). Os hambúrgueres foram mantidos congelados, a ‑18ºC, por 90 dias. Determinou-se o teor de colesterol e a estabilidade oxidativa dos produtos crus e grelhados. Os menores teores de colesterol foram observados nos produtos com óleo de linhaça. No entanto, a adição de linhaça e derivados aumentou a oxidação lipídica em hambúrguer bovino (maiores valores de malonaldeído), após o armazenamento

Reavaliação dos critérios constantes na legislação brasileira para análises de substratos

No Brasil, o Ministério da Agricultura, Pecuária e Abastecimento é o responsável pela legislação que regulamenta as especificações, garantias, tolerâncias, registro, embalagem e rotulagem de substratos para as plantas. Na Instrução Normativa n.º 14 e nas IN nº 17 e 31 estão as exigências quanto aos valores e aos métodos de pH, condutividade elétrica (CE), densidade seca, capacidade de retenção de água (CRA10) e umidade. Os desvios aceitáveis são de ±0,5 para o pH, ±0,3 dS m-1 para a CE, ±15% para densidade seca, até -10% (m/m) para a CRA10 e até +10% para umidade. O objetivo deste trabalho foi avaliar as medidas de pH, CE, densidade seca, CRA10 e umidade de diversos substratos para as plantas, durante o período de seis meses de armazenamento, fornecendo subsídios técnicos para a legislação brasileira. Utilizaram-se nove amostras de substratos comerciais, orgânicas e inorgânicas. Alguns desvios em relação à faixa tolerada pela normativa brasileira foram observados para o pH, CE, CRA10 e umidade em 5,4,6 e 2 amostras respectivamente. Os resultados de densidade seca estavam dentro da faixa permitida pela legislação brasileira. A CRA10 foi a de maior restrição quanto à legislação brasileira, seguida dos valores de pH. Sugere-se o aumento da tolerância para CRA de -15% (m/m) e para o valor de pH±1,0. Além disso, recomenda-se uma reavaliação por parte dos produtores de substratos em relação às matérias-primas constituintes de alguns substratos ou do tempo de armazenamento

S-adenosylmethionine and methylthioadenosine are antiapoptotic in cultured rat hepatocytes but proapoptotic in human hepatoma cells

S-adenosylmethionine (AdoMet) is an essential compound in cellular transmethylation reactions and a precursor of polyamine and glutathione synthesis in the liver. In liver injury, the synthesis of AdoMet is impaired and its availability limited. AdoMet administration attenuates experimental liver damage, improves survival of alcoholic patients with cirrhosis, and prevents experimental hepatocarcinogenesis. Apoptosis contributes to different liver injuries, many of which are protected by AdoMet. The mechanism of AdoMet's hepatoprotective and chemopreventive effects are largely unknown. The effect of AdoMet on okadaic acid (OA)-induced apoptosis was evaluated using primary cultures of rat hepatocytes and human hepatoma cell lines. AdoMet protected rat hepatocytes from OA-induced apoptosis dose dependently. It attenuated mitochondrial cytochrome c release, caspase 3 activation, and poly(ADP-ribose) polymerase cleavage. These effects were independent from AdoMet-dependent glutathione synthesis, and mimicked by 5'-methylthioadenosine (MTA), which is derived from AdoMet. Interestingly, AdoMet and MTA did not protect HuH7 cells from OA-induced apoptosis; conversely both compounds behaved as proapoptotic agents. AdoMet's proapoptotic effect was dose dependent and observed also in HepG2 cells. In conclusion, AdoMet exerts opposing effects on apoptosis in normal versus transformed hepatocytes that could be mediated through its conversion to MTA. These effects may participate in the hepatoprotective and chemopreventive properties of this safe and well-tolerated drug