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The physiological effects of short-term starvation on some haematological, biochemical and non-specific immune response parameters together with the histological structure of the skin, were investigated in the European eel, Anguilla anguilla. Blood haemoglobin and haematocrit, serum glucose and cortisol, hemolysins, haemagglutinins, and lysozyme in the plasma, kidney and epidermal extract, were measured in fish after 31, 42 and 58 days of starvation, and compared to those of fed fish. Starvation did not affect haemoglobin and haematocrit values, while an increase in glucose and cortisol levels was found in starved eels by day 42. Haemolytic and haemagglutinating activities decreased in starved eels. On the other hand, starvation caused an increase in the lysozyme content in the epidermal extracts, while no significant variations were observed in kidney and plasma. On the whole, no major changes in metabolic, haematological and non-specific immune parameters were observed when short-term (less than 2 months) starvation was applied to the European eel, suggesting an adaptive response to starvation, rather than a typical alarm-stress response, allowing this species to withstand food deprivation.

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We have investigated the effects of sex steroids, estradiol (E2), and testosterone (T) on the synthesis of tumor necrosis factor alpha (TNF-alpha) and interleukin-10 (IL-10) in phorbol-myristate-acetate (PMA)-differentiated human monoblastic U937 cells. The ability of both hormones to modulate the viability and programmed cell death of macrophage-like PMA-differentiated U937 cells was also inspected. E2 increased TNF-alpha synthesis, whereas T had no effect on the production of this cytokine. The combination of E2 and its antagonist tamoxifen or ICI-182,789 completely abolished the induction of TNF-alpha, while combination of T and its antagonist Casodex (CSDX) did not significantly affect TNF-alpha production by U937 cells. Exposure of cells to E2 resulted in a dose-dependent decrease of IL-10 synthesis, while again T did not show any detectable effect. In addition, E2 induced a significant increase of apoptosis in macrophage-like U937 cells and this increase was inhibited by the simultaneous addition of either tamoxifen or ICI-182. In contrast, T alone or in combination with CSDX did not modify apoptotic rates of U937 cells. This evidence, taken together, suggests that estrogens, but not androgens, exert a pro-inflammatory action through the modulation of TNF-alpha and IL-10, and regulate the immune effector cells by the induction of programmed cell death.