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This research aims to evaluate the protective effects of combined melatonin and bright light therapy against CNS-oxygen toxicity in nocturnal sand rats.

February 11, 2026

Combined melatonin and bright light therapy mitigate central nervous system oxygen toxicity after day-to-night transition

Key Points

This research aims to evaluate the protective effects of combined melatonin and bright light therapy against CNS-oxygen toxicity in nocturnal sand rats.
Used diurnal and nocturnal sand rat groups for comparison.
Administered different treatments: no treatment, melatonin, bright light therapy, and combination of both.
Performed hyperbaric oxygen exposure to induce CNS-oxygen toxicity and measured latency to onset.
Analyzed urine for 6-sulfatoxymelatonin levels and brain tissue for nNOS and NT levels.
Indoor housing reduced latency to CNS-OT compared to outdoor activity.
Combined treatment of melatonin and light therapy increased latency to CNS-OT to levels similar to daytime activity.
Reduced levels of nNOS and NT in the hippocampus were observed after combined treatment compared to untreated nocturnal group.

Abstract

The greatest risk involved in diving with closed-circuit oxygen rebreather is the development of CNS-oxygen toxicity (CNS-OT), which can be fatal underwater. We previously found in the diurnal model fat sand rat (Psammomys obesus) that night activity is an additional risk factor for CNS-OT. Here, we evaluated protective means which improve the resistance of sand rat to CNS-OT following indoor housing (which cause a shift to nocturnal activity). Five groups of animals were used: one outdoor, day active group (D), and four night active groups composed of (1) indoors group with no treatment (I), (2) indoor group treated with bright light therapy and melatonin (Indoors + light + Mel, ILM), (3) indoor group treated with melatonin only (Indoors + Mel, IM), and (4) indoor group treated only with light therapy (Indoors + Light + IL). The indoors groups underwent 3 weeks of indoor housing. On completion of this term, 6-Sulfatoxymelatonin (6-SMT) levels in urine were determined over a period of 24 h. Animals were then exposed to hyperbaric oxygen (HBO), and we timed the latency to CNS-OT followed by measuring neuronal nitric oxide synthase (nNOS) and nitrotyrosine (NT) levels in the hippocampus. The results indicate that indoor housing (nocturnal activity) shortened the latency to CNS-OT compared to outdoors, diurnal activity. The combined treatment contributed to the elongation of the latency to CNS-OT, which was similar to that of the diurnal group. These changes were accompanied by a significant decrease in hippocampal nNOS and NT levels following the combined treatment compared with the nocturnal group with no treatment. We conclude that the combined treatment may provide protection against CNS-OT in night active sand rats. This protection may partly be attributed to a reduction in hippocampal nNOS and NT levels. Our results indicate that vulnerability to CNS-OT is increased by day-night transition activity and provide new potential treatment for CNS-OT.

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Combined melatonin and bright light therapy mitigate central nervous system oxygen toxicity after day-to-night transition

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