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Protective effects of melatonin against caustic esophageal burn injury in rats
F Larios-Arceo1, G G Ortiz, M Huerta
1Servicio de Cirugía Pediátrica, Hospital de Pediatría, IMSS, Guadalajara, Jalisco, México.
Insights
Melatonin effectively reduced oxidative damage and esophageal tissue changes following corrosive sodium hydroxide burns in rats. This antioxidant may be a promising therapeutic agent for esophageal injury.
Area of Science:
- Biochemistry
- Toxicology
- Pediatric Surgery
Background:
- Caustic ingestion poses a severe risk in children, leading to esophageal structural damage.
- Immediate management and treatment of complications like esophageal strictures are critical.
Purpose of the Study:
- To investigate the potential of melatonin in mitigating esophageal burn damage induced by sodium hydroxide.
- To evaluate melatonin's antioxidant and free radical scavenging properties in this context.
Main Methods:
- Esophageal burns were induced in male rats using 10% sodium hydroxide.
- Lipid peroxidation products (malondialdehyde and 4-hydroxyalkenal) were measured at various time points.
- Tissue hydroxyproline levels were assessed 14 days post-injury.
- Rats received either systemic melatonin or saline, with sham control groups.
Main Results:
- Sodium hydroxide administration rapidly increased lipid peroxidation, indicating free radical involvement.
- Melatonin treatment significantly diminished the oxidative response in the early phase.
- Melatonin also reduced hydroxyproline levels, a marker of tissue damage, in the late phase.
Conclusions:
- Melatonin demonstrates a protective effect against early oxidative damage in sodium hydroxide-induced esophageal burns.
- Melatonin may serve as a potential therapeutic agent to reduce the severity of esophageal injury and its long-term structural complications.
Abstract:
Caustic ingestion is one of the most life-threatening events in the pediatric age group, which requires the immediate management and subsequent treatment of its most significant complication, i.e. alterations in esophageal structure. We investigated whether melatonin could reduce the esophageal burn damage induced by sodium hydroxide. It was assumed that melatonin could be effective because of its function as a direct free radical scavenger, its antioxidative actions and its ability to diminish tissue hydroxyproline (HP) levels. Esophageal burns were induced in male rats by the administration of 10% sodium hydroxide. Lipid peroxidation (LPO) products were then measured at the following times: 0, 1, 6, 24, 48 and 72 hr after treatment. Tissue HP concentrations in the injured area were assessed at 14 days after the administration of sodium hydroxide. The groups received either systemic melatonin or normal saline. There were two, non-ischemic, sham control groups treated with or without melatonin. LPO products, malondialdehyde (MDA) and 4-hydroxyalkenal (4-HDA), increased immediately after the administration of sodium hydroxide; this indicates the participation of free radicals in the development of damage. Melatonin diminished the oxidative response and the amount of HP in the late phase of the lesion. Melatonin reduced oxidative damage in the early phase of the esophageal burns induced by sodium hydroxide.
