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Acetyl-l-Carnitine Attenuates Arsenic-Induced Liver Injury by Abrogation of Mitochondrial Dysfunction, Inflammation, and Apoptosis in Rats
Abstract
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 (5 mg/kg) and arsenic plus ALC (5 mg/kg; 100, 200, 300 mg/kg). The animals were gavaged for 21 consecutive days. Liver tissue samples were extracted 24 h 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 caspase-3 and caspase-9 and initiation of apoptosis, was observed following arsenic administration. Moreover, the inflammation was confirmed by the overexpression of inflammatory mediators such as NF-ĸB and IL-1 and IL-6. The present study demonstrated…
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“Acetyl-L-carnitine is an effective substrate for mitochondrial energy metabolism. Carnitine also has free-radical-scavenging activity that enhances antioxidant status [53]. The hepatoprotective effects of carnitine against various agents, including acetaminophen, sodium valproate, and arsenic, have been proposed and demonstrated [53,54,55].”
From Metabolomic Analysis of Pediatric Patients with Idiosyncratic Drug-Induced Liver Injury According to the Updated RUCAM (2023) · cites this paper as [54]
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Sorted by citations
Andújar-Vera, F., Alés-Palmer, M. L., Muñoz-de-Rueda, P., Iglesias-Baena, I., & Ocete-Hita, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241713562 · Cited by 10
Metadata
- Authors
- Bodaghi-Namileh, V., Sepand, M. R., Omidi, A., Aghsami, M., Seyednejad, S. A., Kasirzadeh, S., & Sabzevari, O.
- Venue
- Environmental Toxicology and Pharmacology
- Publisher
- Elsevier BV
- Published
- 2018-03
- Volume
- 58
- Pages
- 11-20
- ISSN
- 1382-6689
- Cited by
- 78
- References
- 4
- Language
- en
- Funders
- Vice Chancellor for Research
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