Comparative toxicity of allylamine and acrolein in cultured myocytes and fibroblasts from neonatal rat heart

Mechanisms of acrolein-induced myocardial dysfunction: implications for environmental and endogenous aldehyde exposure

“…Acrolein also modified proteins related to energy metabolism, including ATP synthase (␣ and ␤ subunits) and mitochondrial CK-2. These data are consistent with prior studies of acrolein-induced myocardial toxicity (concentrations 5-to 1,500-fold higher than in the present study), demonstrating that millimolar acrolein did not produce morphological changes in the myocardium, but markedly impaired contraction and denatured CK (29) and interfered with energy metabolism and depleted ATP (34). In this context, micromolar acrolein has also been shown to directly impair mitochondrial electron transport and stimulate mitochondrial oxidative stress (20), and mitochondrial ATP synthase is a known target of modification by other lipid peroxidationderived aldehydes (41).…”

Mechanisms of acrolein-induced myocardial dysfunction: implications for environmental and endogenous aldehyde exposure

“…Acrolein also modified proteins related to energy metabolism, including ATP synthase (␣ and ␤ subunits) and mitochondrial CK-2. These data are consistent with prior studies of acrolein-induced myocardial toxicity (concentrations 5-to 1,500-fold higher than in the present study), demonstrating that millimolar acrolein did not produce morphological changes in the myocardium, but markedly impaired contraction and denatured CK (29) and interfered with energy metabolism and depleted ATP (34). In this context, micromolar acrolein has also been shown to directly impair mitochondrial electron transport and stimulate mitochondrial oxidative stress (20), and mitochondrial ATP synthase is a known target of modification by other lipid peroxidationderived aldehydes (41).…”

Protease Activated Receptor-2 Contributes to Heart Failure

“…Pathologic remodeling of the heart in αMHC-PAR-2 mice was accompanied by increased ANF, BNP and βMHC expression and decreased αMHC expression. Importantly, BNP is a strong predictor of cardiac hypertrophy and dysfunction in both mouse models and in humans [24]. During heart hypertrophy, an initial increase in LV wall thickness is usually followed by wall thinning and dilatation of the LV chamber [5].…”

Effects of Amifostine on Glycerol‐Pretreated Rabbit Kidneys

“…On the other hand, acrolein, another degradation product of WR‐1065, may also contribute to the toxicity of amifostine in this study. Cytotoxic effect of acrolein has been shown in various cells (Grafström et al 1988; Torasson et al 1989). Although there are conflicting results about the vascular reactivity, acrolein also attenuates acetylcholine‐induced relaxation in rat thoracic aorta and coronary artery in vitro (Conklin & Boor 1998; Conklin et al 2001; Tsakadzede et al 2003).…”

Mechanisms of acrolein-induced myocardial dysfunction: implications for environmental and endogenous aldehyde exposure

“…Acrolein also modified proteins related to energy metabolism, including ATP synthase (␣ and ␤ subunits) and mitochondrial CK-2. These data are consistent with prior studies of acrolein-induced myocardial toxicity (concentrations 5-to 1,500-fold higher than in the present study), demonstrating that millimolar acrolein did not produce morphological changes in the myocardium, but markedly impaired contraction and denatured CK (29) and interfered with energy metabolism and depleted ATP (34). In this context, micromolar acrolein has also been shown to directly impair mitochondrial electron transport and stimulate mitochondrial oxidative stress (20), and mitochondrial ATP synthase is a known target of modification by other lipid peroxidationderived aldehydes (41).…”

Protease Activated Receptor-2 Contributes to Heart Failure

“…Pathologic remodeling of the heart in αMHC-PAR-2 mice was accompanied by increased ANF, BNP and βMHC expression and decreased αMHC expression. Importantly, BNP is a strong predictor of cardiac hypertrophy and dysfunction in both mouse models and in humans [24]. During heart hypertrophy, an initial increase in LV wall thickness is usually followed by wall thinning and dilatation of the LV chamber [5].…”

Effects of Amifostine on Glycerol‐Pretreated Rabbit Kidneys

“…On the other hand, acrolein, another degradation product of WR‐1065, may also contribute to the toxicity of amifostine in this study. Cytotoxic effect of acrolein has been shown in various cells (Grafström et al 1988; Torasson et al 1989). Although there are conflicting results about the vascular reactivity, acrolein also attenuates acetylcholine‐induced relaxation in rat thoracic aorta and coronary artery in vitro (Conklin & Boor 1998; Conklin et al 2001; Tsakadzede et al 2003).…”

Mechanisms of acrolein-induced myocardial dysfunction: implications for environmental and endogenous aldehyde exposure

“…Acrolein also modified proteins related to energy metabolism, including ATP synthase (␣ and ␤ subunits) and mitochondrial CK-2. These data are consistent with prior studies of acrolein-induced myocardial toxicity (concentrations 5-to 1,500-fold higher than in the present study), demonstrating that millimolar acrolein did not produce morphological changes in the myocardium, but markedly impaired contraction and denatured CK (29) and interfered with energy metabolism and depleted ATP (34). In this context, micromolar acrolein has also been shown to directly impair mitochondrial electron transport and stimulate mitochondrial oxidative stress (20), and mitochondrial ATP synthase is a known target of modification by other lipid peroxidationderived aldehydes (41).…”

Protease Activated Receptor-2 Contributes to Heart Failure

“…Pathologic remodeling of the heart in αMHC-PAR-2 mice was accompanied by increased ANF, BNP and βMHC expression and decreased αMHC expression. Importantly, BNP is a strong predictor of cardiac hypertrophy and dysfunction in both mouse models and in humans [24]. During heart hypertrophy, an initial increase in LV wall thickness is usually followed by wall thinning and dilatation of the LV chamber [5].…”

Effects of Amifostine on Glycerol‐Pretreated Rabbit Kidneys

“…On the other hand, acrolein, another degradation product of WR‐1065, may also contribute to the toxicity of amifostine in this study. Cytotoxic effect of acrolein has been shown in various cells (Grafström et al 1988; Torasson et al 1989). Although there are conflicting results about the vascular reactivity, acrolein also attenuates acetylcholine‐induced relaxation in rat thoracic aorta and coronary artery in vitro (Conklin & Boor 1998; Conklin et al 2001; Tsakadzede et al 2003).…”