Cadmium-induced hepatic endothelial cell injury in inbred strains of mice

The Nitric Oxide Donor, O2-Vinyl 1-(Pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), Protects against Cadmium-Induced Hepatotoxicity in Mice

“…In this regard, the Kupffer cell inhibitor gadolinium chloride blocks Cd-induced hepatotoxicity (Sauer et al, 1998;Harstad and Klaassen, 2002c) and diminishes Cd-induced hepatic radical formation (J. Liu, Q. Guo, M. Waalkes, C. Klaassen, S. Qian, R. Mason, and M. Kadiiska, unpublished data). Cd-induced activation of Kupffer cells could result from endothelial cell damage leading to subsequent ischemia/ congestion, hypoxia, and inflammation (Nolan and Shaikh, 1986;Liu et al, 1992). In the present study, Cd-induced hepatic congestion and inflammation were greatly attenuated by V-PYRRO/NO.…”

The Nitric Oxide Donor, O2-Vinyl 1-(Pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), Protects against Cadmium-Induced Hepatotoxicity in Mice

“…In this regard, the Kupffer cell inhibitor gadolinium chloride blocks Cd-induced hepatotoxicity (Sauer et al, 1998;Harstad and Klaassen, 2002c) and diminishes Cd-induced hepatic radical formation (J. Liu, Q. Guo, M. Waalkes, C. Klaassen, S. Qian, R. Mason, and M. Kadiiska, unpublished data). Cd-induced activation of Kupffer cells could result from endothelial cell damage leading to subsequent ischemia/ congestion, hypoxia, and inflammation (Nolan and Shaikh, 1986;Liu et al, 1992). In the present study, Cd-induced hepatic congestion and inflammation were greatly attenuated by V-PYRRO/NO.…”

Transgenic mouse blastocysts that overexpress metallothionein-I resist cadmium toxicity in vitro

“…Furthermore, it has been reported that Cd2+-induced hepatotoxicity in resistant and sensitive strains of mice does not relate to differences in MT regulation (Quaife et al, 1984;Nolan and Shaikh, 1986;Shaikh et al, 1993). It has also been suggested that Cd2+-induced hepatic endothelial cell injury correlates with strain differences in hepatotoxicity (Liu et al, 1992). It has been noted that CD-1 blastocysts are more resistant to Cd2+ than are B6 blastocysts; this is similar to the sensitivity of these strains to Cd2+-induced teratogenicity (Layton and Layton, 1979).…”

Effect of 5-HT2 Receptor Blockade on Cadmium-Induced Acute Toxicity

“…The degree to which serotonin, through activation of 5-HT 2 receptors, participates in cadmium-induced ischemia is also unknown, but its role may be pronounced. Such a speculation is supported by the fact that in cadmium-treated rats, serotonin acts at sites of the vascular bed with endothelial cell dysfunction or necrosis or apoptosis since endothelial cells represent the most sensitive cell type to the toxic effects of cadmium [48]. From previous experiments by other research groups, it is evident that the vasoconstictive effect of serotonin is extremely intense and pronounced at sites lacking the normal endothelial layer due to elimination of the balancing effect of release of nitric oxide from endothelial cells [48,49].…”

The Nitric Oxide Donor, O2-Vinyl 1-(Pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), Protects against Cadmium-Induced Hepatotoxicity in Mice

“…In this regard, the Kupffer cell inhibitor gadolinium chloride blocks Cd-induced hepatotoxicity (Sauer et al, 1998;Harstad and Klaassen, 2002c) and diminishes Cd-induced hepatic radical formation (J. Liu, Q. Guo, M. Waalkes, C. Klaassen, S. Qian, R. Mason, and M. Kadiiska, unpublished data). Cd-induced activation of Kupffer cells could result from endothelial cell damage leading to subsequent ischemia/ congestion, hypoxia, and inflammation (Nolan and Shaikh, 1986;Liu et al, 1992). In the present study, Cd-induced hepatic congestion and inflammation were greatly attenuated by V-PYRRO/NO.…”

Transgenic mouse blastocysts that overexpress metallothionein-I resist cadmium toxicity in vitro

“…Furthermore, it has been reported that Cd2+-induced hepatotoxicity in resistant and sensitive strains of mice does not relate to differences in MT regulation (Quaife et al, 1984;Nolan and Shaikh, 1986;Shaikh et al, 1993). It has also been suggested that Cd2+-induced hepatic endothelial cell injury correlates with strain differences in hepatotoxicity (Liu et al, 1992). It has been noted that CD-1 blastocysts are more resistant to Cd2+ than are B6 blastocysts; this is similar to the sensitivity of these strains to Cd2+-induced teratogenicity (Layton and Layton, 1979).…”

Effect of 5-HT2 Receptor Blockade on Cadmium-Induced Acute Toxicity

“…The degree to which serotonin, through activation of 5-HT 2 receptors, participates in cadmium-induced ischemia is also unknown, but its role may be pronounced. Such a speculation is supported by the fact that in cadmium-treated rats, serotonin acts at sites of the vascular bed with endothelial cell dysfunction or necrosis or apoptosis since endothelial cells represent the most sensitive cell type to the toxic effects of cadmium [48]. From previous experiments by other research groups, it is evident that the vasoconstictive effect of serotonin is extremely intense and pronounced at sites lacking the normal endothelial layer due to elimination of the balancing effect of release of nitric oxide from endothelial cells [48,49].…”

The Nitric Oxide Donor, O2-Vinyl 1-(Pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), Protects against Cadmium-Induced Hepatotoxicity in Mice

“…In this regard, the Kupffer cell inhibitor gadolinium chloride blocks Cd-induced hepatotoxicity (Sauer et al, 1998;Harstad and Klaassen, 2002c) and diminishes Cd-induced hepatic radical formation (J. Liu, Q. Guo, M. Waalkes, C. Klaassen, S. Qian, R. Mason, and M. Kadiiska, unpublished data). Cd-induced activation of Kupffer cells could result from endothelial cell damage leading to subsequent ischemia/ congestion, hypoxia, and inflammation (Nolan and Shaikh, 1986;Liu et al, 1992). In the present study, Cd-induced hepatic congestion and inflammation were greatly attenuated by V-PYRRO/NO.…”

Transgenic mouse blastocysts that overexpress metallothionein-I resist cadmium toxicity in vitro

“…Furthermore, it has been reported that Cd2+-induced hepatotoxicity in resistant and sensitive strains of mice does not relate to differences in MT regulation (Quaife et al, 1984;Nolan and Shaikh, 1986;Shaikh et al, 1993). It has also been suggested that Cd2+-induced hepatic endothelial cell injury correlates with strain differences in hepatotoxicity (Liu et al, 1992). It has been noted that CD-1 blastocysts are more resistant to Cd2+ than are B6 blastocysts; this is similar to the sensitivity of these strains to Cd2+-induced teratogenicity (Layton and Layton, 1979).…”

Effect of 5-HT2 Receptor Blockade on Cadmium-Induced Acute Toxicity

“…The degree to which serotonin, through activation of 5-HT 2 receptors, participates in cadmium-induced ischemia is also unknown, but its role may be pronounced. Such a speculation is supported by the fact that in cadmium-treated rats, serotonin acts at sites of the vascular bed with endothelial cell dysfunction or necrosis or apoptosis since endothelial cells represent the most sensitive cell type to the toxic effects of cadmium [48]. From previous experiments by other research groups, it is evident that the vasoconstictive effect of serotonin is extremely intense and pronounced at sites lacking the normal endothelial layer due to elimination of the balancing effect of release of nitric oxide from endothelial cells [48,49].…”