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Toxic Responses of the Liver
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
Cholestasis is defined as a reduction of bile formation or impaired secretion of specific bile components. It is not necessarily associated with hepatocyte death, but may be the result of hepatocellular injury or death. Cholestasis can also occur following injury to bile duct cells or blockage of bile ducts. Several toxic agents can induce cholestasis through these mechanisms. Methylene dianiline is one agent that injures bile duct cells and causes cholestasis. Associated with cholestasis is a phenomenon known as jaundice in which the skin and eyes of the affected individual appear yellowish due to the accumulation of bilirubin. Normally the liver degrades hemoglobin, the oxygen-carrying pigment of red blood cells, to a yellowish compound called bilirubin which is excreted with the bile. When bile secretion or flow is reduced, bilirubin accumulates in blood and tissues such as the skin.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
Cholestasis is a reduction of bile formation or impaired secretion of specific bile components. It is not necessarily associated with hepatocyte death, but may be the result of hepatocellular injury or death. Cholestasis can also occur following injury to bile duct cells or blockage of bile ducts. A number of toxic agents can induce cholestasis through these mechanisms. Methylene dianiline is one agent that injures bile duct cells and causes cholestasis. Associated with cholestasis is a phenomenon known as jaundice in which the skin and eyes of the affected individual appear yellowish due to the accumulation of bilirubin. Normally, the liver degrades hemoglobin, the oxygen-carrying pigment of red blood cells, to a yellowish compound called bilirubin which is excreted with the bile. When the secretion or flow is reduced, bilirubin accumulates in blood and tissues, resulting in jaundice.
Ocimum gratissimum (Linn) leaves extract attenuates oxidative stress and liver injury in gentamicin-induced hepatotoxicity in rats
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Oluwadare J. Ogundipe, Omolola F. Akinpelu, Abiodun. Oyerinde, Oyelade R. Oluwakemi
Gentamicin administration increases the activities of these liver enzymes such as AST, ALT and ALP when compared with control. AST and ALT are enzymes found in the liver [21]. AST is found in mitochondrial and cytosol of the liver cells, while ALT is solely cytoplasmic of the liver cells [21]. Therefore, the ameliorating effect of the extracts in the gentamicin-induced alteration in ALT activities suggests that both AOGL and MOGL have cytoplasmic effects that restore the integrity of the membrane of the liver cell. This may be due to the duration of both AOGL and MOGL administration. AOGL and MOGL administration restored the elevated ALP levels. This can be attributed to the extract’s ability to reverse the blockage of the free flow of bile. This is because (cholestasis) obstruction of bile flow in the liver enhances both synthesis and release of hepatic ALP from cell surfaces [21,22]. These are further buttressed by the two weeks treatment recovery.
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Given their critical role in maintaining homeostasis, it is not surprising that gap junctions are frequently involved in pathological conditions (Yamasaki et al. 1999). A wide spectrum of alterations were found in connexin expression and gap junction functionality in liver diseases, including cholestasis (Fallon et al. 1995), nonalcoholic steatohepatitis (Luther et al. 2018), fibrosis (Fischer et al. 2005), cirrhosis (Yang et al. 2019) and liver cancer (Xiang et al. 2019). The nature of the GJIC and/or connexin modifications depends upon the type of cell and disease involved (Hernandez-Guerra, Hadjihambi, and Jalan 2019; Maes et al. 2015a). In acute liver failure (Maes et al. 2016) and hepatitis (Balasubramaniyan et al. 2013), Cx32 and Cx26 production is typically downregulated, while Cx43 expression is upregulated. Generally, Cx43 appears elevated at the expense of Cx32 production in liver disease, owing to both increased production by non-parenchymal cells as well as through de novo expression by hepatocytes (Cooreman et al. 2019).
Indirect clinical markers for the detection of anabolic steroid abuse beyond the conventional doping control in athletes
Published in European Journal of Sport Science, 2019
Georgios A. Christou, Maria A. Christou, Lovro Žiberna, Konstantinos A. Christou
Peliosis hepatis is characterized by blood-filled lacunar spaces within the hepatic parenchyma (Cabasso, 1994; Choi et al., 2009). These lesions vary from minimal asymptomatic to larger massive that may present with cholestasis, liver failure, portal hypertension or even spontaneous rupture (Cabasso, 1994; Choi et al., 2009). Prolonged use of oral AAS for therapeutic indications, such as treatment of aplastic anaemia, has been rarely associated with peliosis hepatis (Choi et al., 2009). Moreover, rare case reports of peliosis hepatis in athletes abusing supratherapeutic doses of AAS have been reported so far (Cabasso, 1994). However, peliosis hepatis in AAS-using athletes may be underreported, because the athletes’ liver is not usually subjected to imaging and thus asymptomatic lesions of peliosis hepatis can be left undiagnosed. Although peliosis hepatis can be occasionally detected in certain morbid conditions, including infections, malignancies and renal failure, the detection of peliosis hepatis in an apparently healthy athlete is highly indicative of chronic AAS abuse.