The cytotoxic and mutagenic properties of cholesterol oxidation products

Lycopene prevents 7-ketocholesterol-induced oxidative stress, cell cycle arrest and apoptosis in human macrophages

“…On the basis of the present study, 7-KC was able to induce oxidative DNA damage, as revealed by the formation of 8-OHdG in human macrophages. These results are in agreement with previous observations that oxysterols, and in particular 7-β-hydroxycholesterol and 7-KC, are mutagenic to Chinese hamster lung fibroblasts [53] since they induce the formation of 8-OHdG, which is considered to be a premutagenic DNA lesion [38]. In the present work, the detection of 8-OHdG thus constitutes a link between the overproduction of ROS and the mutagenicity triggered by 7-KC.…”

Lycopene prevents 7-ketocholesterol-induced oxidative stress, cell cycle arrest and apoptosis in human macrophages

“…On the basis of the present study, 7-KC was able to induce oxidative DNA damage, as revealed by the formation of 8-OHdG in human macrophages. These results are in agreement with previous observations that oxysterols, and in particular 7-β-hydroxycholesterol and 7-KC, are mutagenic to Chinese hamster lung fibroblasts [53] since they induce the formation of 8-OHdG, which is considered to be a premutagenic DNA lesion [38]. In the present work, the detection of 8-OHdG thus constitutes a link between the overproduction of ROS and the mutagenicity triggered by 7-KC.…”

Qualitative and quantitative comparison of the cytotoxic and apoptotic potential of phytosterol oxidation products with their corresponding cholesterol oxidation products

“…Cholestane-3b,5a,6b-triol (triolcholesterol) is reported to be one of the most cytotoxic oxysterols towards rabbit aortic smooth muscle cells (Peng et al 1979), mouse L cells (Higley & Taylor, 1984) and Chinese hamster V79 lung fibroblasts (Sevanian & Peterson, 1986) and its involvement in atherosclerosis has been investigated (Jacobson et al 1985;Matthias et al 1987). We report similar findings.…”

GPCR signaling regulates severe stress‐induced organismic death in Caenorhabditis elegans

“…We note that oac‐31 , like several other oac genes ( oac‐3, 6, 14, 20 ) strongly up‐regulated by FTS (Figure S1g ), encodes a C. elegans homolog of sterol O‐acyltransferase (SOAT). SOAT converts accessible cholesterol into ester forms for storage in lipid droplets (Luo et al, 2020 ; Sevanian & Peterson, 1986 ). While the biochemical function of OAC‐31 remains further characterized, a recent study showed that cold shock can promote lipid movement from the intestine to the germline (Gulyas & Powell, 2021 ).…”

Lycopene prevents 7-ketocholesterol-induced oxidative stress, cell cycle arrest and apoptosis in human macrophages

“…On the basis of the present study, 7-KC was able to induce oxidative DNA damage, as revealed by the formation of 8-OHdG in human macrophages. These results are in agreement with previous observations that oxysterols, and in particular 7-β-hydroxycholesterol and 7-KC, are mutagenic to Chinese hamster lung fibroblasts [53] since they induce the formation of 8-OHdG, which is considered to be a premutagenic DNA lesion [38]. In the present work, the detection of 8-OHdG thus constitutes a link between the overproduction of ROS and the mutagenicity triggered by 7-KC.…”

Qualitative and quantitative comparison of the cytotoxic and apoptotic potential of phytosterol oxidation products with their corresponding cholesterol oxidation products

“…Cholestane-3b,5a,6b-triol (triolcholesterol) is reported to be one of the most cytotoxic oxysterols towards rabbit aortic smooth muscle cells (Peng et al 1979), mouse L cells (Higley & Taylor, 1984) and Chinese hamster V79 lung fibroblasts (Sevanian & Peterson, 1986) and its involvement in atherosclerosis has been investigated (Jacobson et al 1985;Matthias et al 1987). We report similar findings.…”

GPCR signaling regulates severe stress‐induced organismic death in Caenorhabditis elegans

“…We note that oac‐31 , like several other oac genes ( oac‐3, 6, 14, 20 ) strongly up‐regulated by FTS (Figure S1g ), encodes a C. elegans homolog of sterol O‐acyltransferase (SOAT). SOAT converts accessible cholesterol into ester forms for storage in lipid droplets (Luo et al, 2020 ; Sevanian & Peterson, 1986 ). While the biochemical function of OAC‐31 remains further characterized, a recent study showed that cold shock can promote lipid movement from the intestine to the germline (Gulyas & Powell, 2021 ).…”

Lycopene prevents 7-ketocholesterol-induced oxidative stress, cell cycle arrest and apoptosis in human macrophages

“…On the basis of the present study, 7-KC was able to induce oxidative DNA damage, as revealed by the formation of 8-OHdG in human macrophages. These results are in agreement with previous observations that oxysterols, and in particular 7-β-hydroxycholesterol and 7-KC, are mutagenic to Chinese hamster lung fibroblasts [53] since they induce the formation of 8-OHdG, which is considered to be a premutagenic DNA lesion [38]. In the present work, the detection of 8-OHdG thus constitutes a link between the overproduction of ROS and the mutagenicity triggered by 7-KC.…”

Qualitative and quantitative comparison of the cytotoxic and apoptotic potential of phytosterol oxidation products with their corresponding cholesterol oxidation products

“…Cholestane-3b,5a,6b-triol (triolcholesterol) is reported to be one of the most cytotoxic oxysterols towards rabbit aortic smooth muscle cells (Peng et al 1979), mouse L cells (Higley & Taylor, 1984) and Chinese hamster V79 lung fibroblasts (Sevanian & Peterson, 1986) and its involvement in atherosclerosis has been investigated (Jacobson et al 1985;Matthias et al 1987). We report similar findings.…”

GPCR signaling regulates severe stress‐induced organismic death in Caenorhabditis elegans

“…We note that oac‐31 , like several other oac genes ( oac‐3, 6, 14, 20 ) strongly up‐regulated by FTS (Figure S1g ), encodes a C. elegans homolog of sterol O‐acyltransferase (SOAT). SOAT converts accessible cholesterol into ester forms for storage in lipid droplets (Luo et al, 2020 ; Sevanian & Peterson, 1986 ). While the biochemical function of OAC‐31 remains further characterized, a recent study showed that cold shock can promote lipid movement from the intestine to the germline (Gulyas & Powell, 2021 ).…”