Biotransformations, Antioxidant System Responses, and Histopathological Indexes in the Liver of Fish Exposed to Cyanobacterial Extract

Abstract

Radiocystis fernandoi, a microcystin (MC) producer, has been common in cyanobacterial blooms in tropical regions. Microcystin is a hepatotoxin that causes tissue damage and even death in animals, including humans; its detoxification process may involve biotransformation and activation of the antioxidant defense system. We evaluated the detoxification pathway, examined the antioxidant defense system responses, and determined the alterations and the organ histopathological indexes in the liver of the tropical fish Hoplias malabaricus after acute and subchronic intraperitoneal exposure to microcystin. The crude microcystin extract of R. fernandoi had predominantly MC‐RR and MC‐YR. The detoxification process was activated by increasing ethoxyresorufin‐O‐deethylase activity, whereas glutathione S‐transferase was inhibited. The activity of the antioxidant defense enzymes superoxide dismutase (SOD) and glutathione peroxidase decreased after acute exposure; the SOD–catalase system and the glutathione level increased after subchronic exposure. The carbonyl protein level, lipid peroxidation (LPO), and DNA damage were unchanged after acute exposure, whereas protein carbonyl was unchanged, LPO decreased, and DNA damage increased after subchronic exposure. Histopathological alteration indexes differed between acute and subchronic exposure, but the histopathological organ indexes indicate liver dysfunction in both exposure periods. We conclude that MC‐RR and MC‐YR induce different liver responses depending on the time of exposure, and the antioxidant defense responses after subchronic exposure may help to partially restore the liver function. Environ Toxicol Chem 2020;39:1041–1051. © 2020 SETAC

The Protective Effects of Zornia diphylla (L.) Pers. Against Acute Liver Injury Induced by Carbon Tetrachloride in Mice

“…When hepatocytes are attacked by free radicals, SOD can be reduced due to its excessive consumption. The reduction in its activity can lead to the accumulation of oxygen free radicals in the body, resulting in peroxidation of plasma membrane, damage to the membrane structure and function, and finally to the death of hepatocytes (Sun et al, 2010;Saeedi Saravi et al, 2016;Paulino et al, 2020). MDA is a special marker of oxidative damage.…”

Liver dysfunction and energy storage mobilization in traíra, Hoplias malabaricus (Teleostei, Erythrinidae) induced by subchronic exposure to toxic cyanobacterial crude extract

“…The short‐term (up to 96 h) exposure to CE of R fernandoi R28 strain causes prompt impairment in the fish liver which is clearly supported by the morphological/histopathological and biochemical alterations in this organ. The loss of hepatocyte shape (from polygonal to round form), nuclear alterations, swelling of mitochondria, whirling of ER, enlargement of sinusoids, and hyperemia in the liver were the major histological and ultrastructural changes characterized by CE MC‐content toxicity 12,15,16 . The changes in the activity of biotransformation and antioxidant systems, the enzyme activity that constitutes the biomarkers of liver function evidenced the tissue response to the toxins present in the crude extract and indicate different degrees of organ dysfunction 15,16,21 which is accompanied by adjustments in the energetic metabolism 21 …”

“…MC are specific inhibitor of protein phosphatase 1 and 2A and transported into liver by organic anions polypeptides transporter (OATPs) 13 . MC also induces the production of reactive oxygen species, disorganization of the hepatocyte cytoskeleton resulting in liver pathology, intrahepatic hemorrhage and hypovolemic shock which can cause animals and human death 12–17 . The impairing liver tissue affects their functions and increases the energetic demand 18,19 .…”

“…Previous investigation of crude extract (CE) of R. fernandoi , strain R28, in the liver of the neotropical fish Hoplias malabaricus after short (12 and 96 h)‐ and long (30 d)‐term intraperitoneal exposure evidenced differences in MC‐YR and MC‐RR bioaccumulation, biotransformation enzyme activity, antioxidant responses and morphological effects depending on time‐exposure 12,16 . Short‐term exposure induced changes in the acid and alkaline phosphatase activity, and in the aminotransferases, key enzymes for metabolic processes, as well as in intermediate metabolites 21 and in hepatic bile biomarkers 24 …”

“…13 MC also induces the production of reactive oxygen species, disorganization of the hepatocyte cytoskeleton resulting in liver pathology, intrahepatic hemorrhage and hypovolemic shock which can cause animals and human death. [12][13][14][15][16][17] The impairing liver tissue affects their functions and increases the energetic demand. 18,19 In fish, the MC effects in the energetic metabolism are poorly exploited and there are few studies reporting an integrated metabolic pathway.…”