Hepatic Pathological Changes Due to Hydroxyalkenals

Wilson, Dennis W; Segall, H. J.; Lamé, Michael W.

doi:10.1007/978-1-4684-5134-4_81

Cited by 3 publications

(2 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently our laboratory isolated trans-4-OH-2-hexenal (t-4HH) from the hepatic microsomal metabolism of senecionine (Segall et al, 1985). When t-4HH was injected as a lipid suspension into the portal vein of rats, hepatic necrosis was produced which appeared to be similar to that elicited by the injection of senecionine (Segall et al, 1985;Wilson et al, 1986). In addition, t-4HH has also been shown to cause cytotoxicity and genotoxicity in primary cultures of rat hepatocytes (Griffin and Segall, 1986).…”

Section: Introductionmentioning

confidence: 93%

Lipid peroxidation and cellular damage caused by the pyrrolizidine alkaloid senecionine, the alkenal trans-4-hydroxy-2-hexenal, and related alkenals

Griffin

Segall

1987

Cell Biol Toxicol

Self Cite

View full text Add to dashboard Cite

Lipid peroxidation was examined as a possible mechanism for cell injury by trans-4-OH-2-hexenal, the macrocyclic pyrrolizidine alkaloid senecionine and related alkenals in isolated rat hepatocytes. Each compound elicited a positive dose response for peroxidation of cellular lipids as measured by the formation of thiobarbituric acid-reactive products. The addition of the anti-oxidant N,N'-diphenyl-p-phenylenediamine to the hepatocyte suspensions inhibited the production of thiobarbituric acid-reactants. However, the presence of the anti-oxidant had no protective effects on the cell membrane integrity as evidenced by the leakage of lactate dehydrogenase from the cells into the surrounding media. These results suggest that lipid peroxidation which occurs in the presence of senecionine, trans-4-OH-2-hexenal or related alkenals is not entirely responsible for the cellular damage in isolated rat hepatocytes.

show abstract