Acetyl-l-carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats

Publication date: Available online 12 December 2017 Source:Environmental Toxicology and Pharmacology Author(s): Vida Bodaghi-Namileh, Mohammad Reza Sepand, Ameneh Omidi, Mehdi Aghsami, Seyed Afshin Seyednejad, Sara Kasirzadeh, Omid Sabzevari Industrial and agricultural developments in recent years have resulted in the excessive discharge of arsenic into the environment, making arsenic toxicity a major worldwide concern. Oxidative stress is considered the primary mechanism for arsenic toxicity. The main objective of this study was to evaluate acetyl-l-carnitine’s (ALC) protective ability against the arsenic-induced hepatotoxicity. For this purpose, male Wistar rats were distributed randomly into 5 groups of 8 rats each: control, Arsenic (5mg/kg) and arsenic plus ALC (5mg/kg; 100, 200, 300mg/kg). The animals were gavaged for 21 consecutive days. Liver tissue samples were extracted 24h after the last treatment and were later analyzed for biochemical and histological alterations. The arsenic-induced oxidative damage was confirmed by elevation of malondialdehyde (MDA), a lipid peroxidation byproduct, as well as depletion in physiological antioxidant content such as superoxide dismutase (SOD) and catalase (CAT). Furthermore, alterations in mitochondrial functions including a significant decrease of mitochondrial outer membrane potential and reactive oxygen species (ROS) generation increase, mitochondrial swelling, release of cytochrome c and consequent activation of casp...
Source: Environmental Toxicology and Pharmacology - Category: Environmental Health Source Type: research