Steroids in hepatic failure

There is a more recent school of thought that indicates activation of the androgen receptors in the liver itself (aggravated by the potency of the steroid), and inducement of reactive oxygen species (ROS) are causative factors in the liver toxicity of a given oral anabolic steroid – and this may be true, because something like methyltrienolone is incredibly potent at lower doses than any other steroid, but is very liver toxic, while Anavar (oxandrolone) isn’t very liver toxic at all, and requires significantly higher doses for users to experience tangible results.

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Bodybuilders, who abuse anabolic androgen steroids over a long period of time have a great risk of developing an HCA or HCC and should therefore be well monitored. Periodic hepatic ultrasound seems to be an adequate screening procedure to detect the development of hepatic lesions [ 13 ]. Although most of the tumors developing by AAS misuse or intake of oral contraceptives are benign, early detection is important in order to avoid the associated risk of malignant transformation and life-threatening haemorrhages [ 14 ]. In these cases a surgical excision is recommended [ 5 , 13 ]. A nonsurgical approach for these tumors has also been suggested because of the regression of some tumors after stopping the medication. In contrast to this observation, a recurrence and enlargement have been reported in cases where steroids have been continued [ 9 , 15 ].

Primary hepatocytes are commonly used in cell biological and biopharmaceutical research. In vitro model systems based on hepatocytes have been of great help to better understand the role of hepatocytes in (patho)physiological processes of the liver. In addition, pharmaceutical industry has heavily relied on the use of hepatocytes in suspension or culture to explore mechanisms of drug metabolism and even predict in vivo drug metabolism. For these purposes, hepatocytes are usually isolated from animal or human [5] whole liver or liver tissue by collagenase digestion, which is a two-step process. In the first step, the liver is placed in an isotonic solution, in which calcium is removed to disrupt cell-cell tight junctions by the use of a calcium chelating agent . Next, a solution containing collagenase is added to separate the hepatocytes from the liver stroma . This process creates a suspension of hepatocytes, which can be seeded in multi-well plates and cultured for many days or even weeks. For optimal results, culture plates should first be coated with an extracellular matrix (. collagen, Matrigel) to promote hepatocyte attachment (typically within 1-3 hr after seeding) and maintenance of the hepatic phenotype. In addition, and overlay with an additional layer of extracellular matrix is often performed to establish a sandwich culture of hepatocytes. The application of a sandwich configuration supports prolonged maintenance of hepatocytes in culture. [6] [7] Freshly-isolated hepatocytes that are not used immediately can be cryopreserved and stored. [8] They do not proliferate in culture. Hepatocytes are intensely sensitive to damage during the cycles of cryopreservation including freezing and thawing. Even after the addition of classical cryoprotectants there is still damage done while being cryopreserved. [9] Nevertheless, recent cryopreservation and resuscitation protocols support application of cryopreserved hepatocytes for most biopharmaceutical applications. [10]

AB - The effects of various hypothalamic lesions on hepatic steroid metabolism in adult rats were investigated. It was found that frontal deafferentation at the retrochiasmatic and suprachiasmatic level resulted in a complete 'feminization' of hepatic steroid metabolism in male rats. Such an effect was also seen when lesions involving mainly the anterior periventricular hypothalamic area and the suprachiasmatic nucleus were performed in male rats. Midline lesions, anterior to the suprachiasmatic nucleus, on the other hand, did not result in any significant effects. A moderate degree of 'feminization' was obtained after bilateral lesions involving mainly the nucleus interstitialis striae terminalis but including also parts of the anterior commissure. Small lesions in the lateral preoptic area were, however, without effect. No effects were seen of analogous lesions in female rats in any of the cases studied. The present findings suggest that a region including the anterior hypothalamic periventricular area, the suprachiasmatic nucleus and adjacent areas is involved in the control of hepatic steroid metabolism. It is postulated that the neuronal cell bodies that produce a factor with an inhibitory effect on the secretion of 'feminizing factor' have their origins in this area of the hypothalamus, or, alternatively, may send axons through this area to the basal hypothalamus and thus directly or indirectly influence the anterior pituitary gland.

Steroids in hepatic failure

steroids in hepatic failure

Primary hepatocytes are commonly used in cell biological and biopharmaceutical research. In vitro model systems based on hepatocytes have been of great help to better understand the role of hepatocytes in (patho)physiological processes of the liver. In addition, pharmaceutical industry has heavily relied on the use of hepatocytes in suspension or culture to explore mechanisms of drug metabolism and even predict in vivo drug metabolism. For these purposes, hepatocytes are usually isolated from animal or human [5] whole liver or liver tissue by collagenase digestion, which is a two-step process. In the first step, the liver is placed in an isotonic solution, in which calcium is removed to disrupt cell-cell tight junctions by the use of a calcium chelating agent . Next, a solution containing collagenase is added to separate the hepatocytes from the liver stroma . This process creates a suspension of hepatocytes, which can be seeded in multi-well plates and cultured for many days or even weeks. For optimal results, culture plates should first be coated with an extracellular matrix (. collagen, Matrigel) to promote hepatocyte attachment (typically within 1-3 hr after seeding) and maintenance of the hepatic phenotype. In addition, and overlay with an additional layer of extracellular matrix is often performed to establish a sandwich culture of hepatocytes. The application of a sandwich configuration supports prolonged maintenance of hepatocytes in culture. [6] [7] Freshly-isolated hepatocytes that are not used immediately can be cryopreserved and stored. [8] They do not proliferate in culture. Hepatocytes are intensely sensitive to damage during the cycles of cryopreservation including freezing and thawing. Even after the addition of classical cryoprotectants there is still damage done while being cryopreserved. [9] Nevertheless, recent cryopreservation and resuscitation protocols support application of cryopreserved hepatocytes for most biopharmaceutical applications. [10]

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