Quercetin attenuates cadmium-induced hepatotoxicity by suppressing oxidative stress and apoptosis in rat.

Background: Cadmium (Cd) is considered a major industrial and environmental toxicant, threatening the health of aquatic organisms, plants, animals, and humans. Quercetin (Que) is a natural flavonoid with antioxidant properties. The purpose of this study was to investigate the role of the oxidative stress and apoptosis in Cd-induced hepatotoxicity and the protective effect of Que.

Protective effect of naringenin on cadmium chloride-induced renal injury via alleviating oxidative stress, endoplasmic reticulum stress, and autophagy in chickens.

Cadmium (Cd) is a highly hazardous toxic substance that can cause serious harm to animals. Previous studies have indicated that cadmium chloride (CdCl) can damage organs, such as the liver, ovaries, and testicles. Naringenin (Nar) represents a flavonoid with various properties that promote the alleviation of Cd-induced damage.

Roles of Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway in Cd-induced testicular injury in rats and the protective effect of quercetin.

Cadmium (Cd) exposure causes oxidative damage to mitochondria, which would adversely affect rat testicular tissue. Quercetin (Que) is a natural antioxidant with anti-inflammatory, antioxidant and anti-apoptotic effects. However, the mechanism by which Que inhibits Cd-induced apoptosis of testicular cells remains unclear.