The aldehyde 4-hydroxynonenal (HNE), peroxidation product of polyunsaturated fatty acids is considered the most reliable indicator of endogenous lipid peroxidation in vivo (1). Lipid peroxidation is an autocatalytic mechanism leading to oxidative destruction of cellular membranes. Oxidative stress is epiphenomenon of hepatitis and pathogenic factor of liver cirrhosis, while HNE acts as growth regulating factor and signaling molecules (2). The aim of present study was to investigate the presence of HNE-modified proteins in human and in animal cirrhotic liver by immunohistochemistry. 30 fixed paraffin-embedded liver samples with cirrhosis were retrospectively selected for the study. There were 4 cases of cardiac liver cirrhosis in dogs, and 30 cases of various human chronic liver diseases in stage of cirrhosis. There were 15 cases of chronic hepatitis C and B, 4 cases of hemochromatosis, 4 cases of Wilson's disease and 3 cases of alcoholic cirrhosis. Slides of paraffin-embedded tumor tissue were prepared for immunohistochemistry with monoclonal antibodies to HNE-histidine conjugate. Positive immunohistochemical reaction to HNE was analyzed semi-quantitatively. Intracellular HNE adduct localized in the cytoplasm of hepatocytes was detected respectively in 25 of 30 cases (83%).The strongest staining was noticed in cases of Wilson’s disease, hemochromatosis, alcoholic liver diseases and cardiac liver cirrhosis in dogs. Weak staining was observed in cases of chronic hepatitis C and B. The results of the study indicate that HNE can be detected in several chronic human and in animal liver diseases. Therefore, detection of lipid peroxidation could be used in predicting development of fibrosis and cirrhosis in chronic liver diseases.
This study used malondialdehyde (MDA) determination by HPLC and enzymatic assays for total serum peroxides and antioxidant capacity to evaluate oxidative stress in 47 healthy full-term small-for-gestational age (SGA) newborns vs 67 appropriate-for-gestational age (AGA) newborns. Blood samples were collected at delivery from umbilical cord artery and vein and from peripheral blood of the babies on the third day after birth. Blood samples of mothers were also collected and compared with blood of 29 normal non-pregnant women (NPW). Serum peroxide values were significantly higher in both groups of mothers than in NPW, decreasing towards the third day in AGA mothers, while persisting in SGA mothers. Antioxidant capacity of sera of both groups of mothers was lower than NPW. Both SGA mothers and babies had increased MDA at delivery, unlike AGA counterparts. MDA levels in umbilical vein were higher than in umbilical arteries, while immunohistochemistry revealed abundant presence of 4-hydroxynonenal (HNE)-protein adducts only in stroma of the SGA placenta. These results show that both mothers and babies are exposed to oxidative stress during and after delivery, which is more pronounced and persistent in the perinatal period of the SGA group, while lipid peroxidation in placenta could play a role in SGA pathophysiology.
Abstract Aging is a multi‐factorial process which involves deprivation in body's metabolism. Brain mitochondria are prone to oxidative damage owing to their high metabolic rate. The decline in antioxidant system during aging augments the neuronal damage to mitochondrial components like antioxidant system, Kreb's cycle enzymes and electron transport chain complexes. Since brain is an organ rich in fatty acids, lipid peroxidation products like hydroxynonenal are predominant. Those lipid peroxidation products conjugate with amino acids to form adducts which alter their structural and functional properties. Epigallo catechin gallate is a potent antioxidant which is rich in green tea extract. This study elucidated the antioxidant potential of epigallo catechin gallate to counteract the mitochondrial oxidative damage in brain. The study comprised of young (3–4 months old; 150 ± 20 g) and aged (above 24 months; 420 ± 20 g) male albino rats of Wistar strain in Groups I and II. Groups III and IV comprised of young and aged rats supplemented with epigallo catechin gallate (2 mg/kg body weight) for 30 days. Antioxidants, Kreb's cycle enzymes and electron transport chain complexes were assayed in the mitochondrial fraction. Hydroxynonenal expression was carried out using immunohistochemical analysis. Epigallo catechin gallate supplementation decreased the expression of hydroxynonenal in aged brain, up‐regulated the antioxidant system and augmented the activities of Kreb's cycle enzymes and electron transport chain complexes in aged brain mitochondria thus proving its antioxidant potential at the level of mitochondria.