Melanomacrophage centres (MMCs) play a key role in the immune response in fish. They are considered sensitive bio-monitoring structures with roles in the assessment of toxicant impacts. The aim of this study was to examine the potential histopathological effect of 4-nonylphenol (4-NP) on hepatic MMCs in Clarias gariepinus. To achieve this objective, adult male fish were divided randomly and equally into two groups: a control group and a group that was exposed to 4-NP (dissolved in water at a dose of 0.1 mg/L) for 21 days. The 4-NP-intoxicated hepatic MMCs contained numerous necrotic macrophages. Superoxide dismutase 2 was immuno-expressed in the hepatic MMCs in both groups, with no significant difference. Histomorphometric examination revealed that the sizes and numbers of MMCs were dramatically higher in the livers of 4-NP-exposed C. gariepinus than in control fish. Following 4-NP challenge, in the liver, the abundance of lipofuscin and haemosiderin pigments increased, and single-pigmented macrophages, aggregated groups of deformed red blood cells (RBCs) and macrophages were present near blood vessels and hepatic sinusoids. These results reveal that 4-NP exerts immunological effects on hepatic MMCs in C. gariepinus and support the utility of MMCs as a cytological biomarker for aquatic exposure to 4-NP.

4-Nonylphenol (NP) toxicity in fish attracts much attention due to its ability in targeting several organs; however, the researches regarding its potential hepatotoxicity are conflicting and still require further investigation. Therefore, the objective of this study is to focus on this issue from the histophysiological point of view using NP intoxicated African catfish (Clarias gariepinus) as a model of hepatotoxicity. Twelve adult fish (6 per group) were divided into two groups; the first was considered as a control and the second was exposed to NP dissolved in water at a dose of 0.1 mg/kg BW for 3 weeks. A significant reduction in the hepatic alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase levels was observed in NP-exposed fish. Concerning the oxidant/antioxidant balance, a significant depletion in superoxide dismutase, catalase, and glutathione peroxidase was found along with a significant elevation in total peroxide and malondialdhyde. The histopathological examination of the hepatic tissues revealed that NP had marked hepatotoxic effects including hepatitis, centrilobular and focal hydropic and fatty degeneration, fatty change (steatosis), hepatic coagulative necrosis, and nuclear alterations in addition to apoptosis of hepatocytes and necrosis of endothelial cells. Depletion of the glycogen and increased in pigments (lipofuscin and hemosiderin) content in the hepatocytes were also recorded. Hemosiderosis and proliferation of the connective tissue around the blood vessels and branches of bile ducts and in the portal areas were also observed. In light of these findings, it was concluded that NP has a well-defined hepatotoxic impact paving the road towards other studies to investigate other detrimental cyto-physiological influences of this aquatic pollutant.

4-Nonylphenol (NP) toxicity in fish attracts much attention due to its ability in targeting several organs; however, the researches regarding its potential hepatotoxicity are conflicting and still require further investigation. Therefore, the objective of this study is to focus on this issue from the histophysiological point of view using NP intoxicated African catfish (Clarias gariepinus) as a model of hepatotoxicity. Twelve adult fish (6 per group) were divided into two groups; the first was considered as a control and the second was exposed to NP dissolved in water at a dose of 0.1 mg/kg BW for 3 weeks. A significant reduction in the hepatic alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase levels was observed in NP-exposed fish. Concerning the oxidant/antioxidant balance, a significant depletion in superoxide dismutase, catalase, and glutathione peroxidase was found along with a significant elevation in total peroxide and malondialdhyde. The histopathological examination of the hepatic tissues revealed that NP had marked hepatotoxic effects including hepatitis, centrilobular and focal hydropic and fatty degeneration, fatty change (steatosis), hepatic coagulative necrosis, and nuclear alterations in addition to apoptosis of hepatocytes and necrosis of endothelial cells. Depletion of the glycogen and increased in pigments (lipofuscin and hemosiderin) content in the hepatocytes were also recorded. Hemosiderosis and proliferation of the connective tissue around the blood vessels and branches of bile ducts and in the portal areas were also observed. In light of these findings, it was concluded that NP has a well-defined hepatotoxic impact paving the road towards other studies to investigate other detrimental cyto-physiological influences of this aquatic pollutant.

4-Nonylphenol (NP) toxicity in fish attracts much attention due to its ability in targeting several organs; however, the researches regarding its potential hepatotoxicity are conflicting and still require further investigation. Therefore, the objective of this study is to focus on this issue from the histophysiological point of view using NP intoxicated African catfish (Clarias gariepinus) as a model of hepatotoxicity. Twelve adult fish (6 per group) were divided into two groups; the first was considered as a control and the second was exposed to NP dissolved in water at a dose of 0.1 mg/kg BW for 3 weeks. A significant reduction in the hepatic alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase levels was observed in NP-exposed fish. Concerning the oxidant/antioxidant balance, a significant depletion in superoxide dismutase, catalase, and glutathione peroxidase was found along with a significant elevation in total peroxide and malondialdhyde. The histopathological examination of the hepatic tissues revealed that NP had marked hepatotoxic effects including hepatitis, centrilobular and focal hydropic and fatty degeneration, fatty change (steatosis), hepatic coagulative necrosis, and nuclear alterations in addition to apoptosis of hepatocytes and necrosis of endothelial cells. Depletion of the glycogen and increased in pigments (lipofuscin and hemosiderin) content in the hepatocytes were also recorded. Hemosiderosis and proliferation of the connective tissue around the blood vessels and branches of bile ducts and in the portal areas were also observed. In light of these findings, it was concluded that NP has a well-defined hepatotoxic impact paving the road towards other studies to investigate other detrimental cyto-physiological influences of this aquatic pollutant.

NULL

NULL

NULL

NULL

NULL

NULL