Maintaining a balanced Bcl-2/Bax ratio and increased antioxidant capacity in tissue and mitochondria inhibits apoptosis in goose fatty liver.

1. Apoptosis is suppressed in the formation of goose fatty liver, which may be a protective mechanism. The objective of this study was to elucidate the mechanism by which apoptosis is inhibited in goose fatty liver.2. Twenty, male, Landes geese were selected and randomly divided into a control group and an overfed treatment. Additionally, the primary hepatocytes were isolated from the goose embryos and treated with glucose.3. The geese in the overfed group had higher liver weight, body weight and liver:body weight ratio than that in the control (p < 0.05). No significant difference on inflammation, fibrillation, or apoptosis level was observed from the staining of liver sections between the control and overfed group.4. Neither the protein level of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X (Bax) in liver nor the malondialdehyde concentration and manganese superoxide dismutase activity in liver mitochondria was altered in these two treatments (p < 0.05). Compared with the control group, the overfed treatment had decreased reduced glutathione (GSH) and increased glutathione reductase activity in liver mitochondria (p < 0.05).5. There was no significant difference in apoptosis level, Bcl-2 and Bax protein level and Bcl-2/Bax ratio was found in hepatocytes treated with 20, 40 or 60 mM glucose when compared with the control group (p < 0.05). However, treatment with 40 or 60 mM glucose tended to increase the MDA concentration in hepatocytes (p = 0.055 and p = 0.091, respectively). The hepatocytes in 40 or 60 mM glucose treatment had decreased GSH concentration in comparison to the control (p < 0.05).6. These findings suggested that apoptosis inhibition in goose fatty liver may be mediated through maintenance of Bcl-2/Bax ratio. Additionally, the increased antioxidant ability in tissue and mitochondria of goose fatty liver may contribute to resistance of apoptosis.