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Identify Melatonin as a Novel Therapeutic Reagent in the Treatment of 1-Bromopropane(1-BP) Intoxication

View Article: PubMed Central - PubMed

ABSTRACT

1-Bromopropane (1-BP) has been used as an alternative for fluoride compounds and 1-BP intoxication may involve lung, liver, and central neural system (CNS). Our previous studies showed that 1-BP impaired memory ability by compromising antioxidant cellular defenses. Melatonin is a powerful endogenous

antioxidant, and the objective of this study was to explore the therapeutic role of melatonin in the treatment of 1-BP intoxication. Rats were intragastrically treated with 1-BP with or without melatonin, and then sacrificed on 27th day after 1-BP administration. The Morris water maze (MWM) test was used to evaluate the spatial learning and memory ability of the experimental animals, and NeuN staining was performed to assess neuron loss in hippocampus. We found that rats treated with 1-BP spent more time and swam longer distance before landing on the hidden platform with a comparable swimming speed, which was markedly mitigated by the pretreatment with melatonin in a concentration-dependent manner. In addition, 1-BP-induced notable decrease in neuron population in hippocampus by promoting apoptosis, and melatonin pretreatment attenuated those changes in brain. The GSH/GSSG ratio was proportionately decreased and heme oxygenase 1 was increased in the rats exposed to 1-BP (Figure 6), and administration of melatonin restored them. Meanwhile, MDA, the level of lipid peroxidation product, was significantly increased upon exposed to 1-BP, which was significantly attenuated by melatonin pretreatment, indicating that administration of 1-BP could interfere with redox homeostasis of brain in rat, and such 1-BP-induced biomedical changes were reversed by treatment with melatonin.

We conclude that treatment with melatonin attenuates 1-BP-induced CNS toxicity through its ROS scavenging effect.

No MeSH data available.


Related in: MedlinePlus

Effects of melatonin on 1-bromopropane(1-BP) induced lipid oxidation stress in cerebral cortex of SD rats. Data were shown as mean ± SEM (n = 10). (A) The GSH/GSSG ratio of cerebral cortex in SD rats. (B) The malondialdehyde (MDA) measurement of cortex in SD rats. (C)The expression of HO1 was notably upregulated upon exposure to 1-BP and was attenuated by the treatment of melatonin. ∗P < 0.05, ∗∗P < 0.01, nsP > 0.05 versus 1-BP group£»##P < 0.01 versus control group. 1-BP = 1-bromopropane, MDA = malondialdehyde, SD rats = Sprague-Dawley rats.
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Figure 6: Effects of melatonin on 1-bromopropane(1-BP) induced lipid oxidation stress in cerebral cortex of SD rats. Data were shown as mean ± SEM (n = 10). (A) The GSH/GSSG ratio of cerebral cortex in SD rats. (B) The malondialdehyde (MDA) measurement of cortex in SD rats. (C)The expression of HO1 was notably upregulated upon exposure to 1-BP and was attenuated by the treatment of melatonin. ∗P < 0.05, ∗∗P < 0.01, nsP > 0.05 versus 1-BP group£»##P < 0.01 versus control group. 1-BP = 1-bromopropane, MDA = malondialdehyde, SD rats = Sprague-Dawley rats.

Mentions: As shown in Figure 6A, the GSH/GSSG ratio was proportionately decreased in the rats exposed to 1-BP (Figure 6), and administration of melatonin restored the level of the GSH/GSSG ratio. Meanwhile, MDA, the level of lipid peroxidation product, was significantly increased upon exposed to 1-BP, which was significantly attenuated by melatonin pretreatment, indicating that administration of 1-BP could interfere with redox homeostasis of brain in rat, and such 1-BP-induced biomedical changes were reversed by treatment with melatonin. Furthermore, we determined the expression of HO1 using western blot analysis. As shown in Figure 6C, the expression of HO1 was notably upregulated upon exposure to 1-BP and was attenuated by the treatment of melatonin.


Identify Melatonin as a Novel Therapeutic Reagent in the Treatment of 1-Bromopropane(1-BP) Intoxication
Effects of melatonin on 1-bromopropane(1-BP) induced lipid oxidation stress in cerebral cortex of SD rats. Data were shown as mean ± SEM (n = 10). (A) The GSH/GSSG ratio of cerebral cortex in SD rats. (B) The malondialdehyde (MDA) measurement of cortex in SD rats. (C)The expression of HO1 was notably upregulated upon exposure to 1-BP and was attenuated by the treatment of melatonin. ∗P < 0.05, ∗∗P < 0.01, nsP > 0.05 versus 1-BP group£»##P < 0.01 versus control group. 1-BP = 1-bromopropane, MDA = malondialdehyde, SD rats = Sprague-Dawley rats.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4998236&req=5

Figure 6: Effects of melatonin on 1-bromopropane(1-BP) induced lipid oxidation stress in cerebral cortex of SD rats. Data were shown as mean ± SEM (n = 10). (A) The GSH/GSSG ratio of cerebral cortex in SD rats. (B) The malondialdehyde (MDA) measurement of cortex in SD rats. (C)The expression of HO1 was notably upregulated upon exposure to 1-BP and was attenuated by the treatment of melatonin. ∗P < 0.05, ∗∗P < 0.01, nsP > 0.05 versus 1-BP group£»##P < 0.01 versus control group. 1-BP = 1-bromopropane, MDA = malondialdehyde, SD rats = Sprague-Dawley rats.
Mentions: As shown in Figure 6A, the GSH/GSSG ratio was proportionately decreased in the rats exposed to 1-BP (Figure 6), and administration of melatonin restored the level of the GSH/GSSG ratio. Meanwhile, MDA, the level of lipid peroxidation product, was significantly increased upon exposed to 1-BP, which was significantly attenuated by melatonin pretreatment, indicating that administration of 1-BP could interfere with redox homeostasis of brain in rat, and such 1-BP-induced biomedical changes were reversed by treatment with melatonin. Furthermore, we determined the expression of HO1 using western blot analysis. As shown in Figure 6C, the expression of HO1 was notably upregulated upon exposure to 1-BP and was attenuated by the treatment of melatonin.

View Article: PubMed Central - PubMed

ABSTRACT

1-Bromopropane (1-BP) has been used as an alternative for fluoride compounds and 1-BP intoxication may involve lung, liver, and central neural system (CNS). Our previous studies showed that 1-BP impaired memory ability by compromising antioxidant cellular defenses. Melatonin is a powerful endogenous

antioxidant, and the objective of this study was to explore the therapeutic role of melatonin in the treatment of 1-BP intoxication. Rats were intragastrically treated with 1-BP with or without melatonin, and then sacrificed on 27th day after 1-BP administration. The Morris water maze (MWM) test was used to evaluate the spatial learning and memory ability of the experimental animals, and NeuN staining was performed to assess neuron loss in hippocampus. We found that rats treated with 1-BP spent more time and swam longer distance before landing on the hidden platform with a comparable swimming speed, which was markedly mitigated by the pretreatment with melatonin in a concentration-dependent manner. In addition, 1-BP-induced notable decrease in neuron population in hippocampus by promoting apoptosis, and melatonin pretreatment attenuated those changes in brain. The GSH/GSSG ratio was proportionately decreased and heme oxygenase 1 was increased in the rats exposed to 1-BP (Figure 6), and administration of melatonin restored them. Meanwhile, MDA, the level of lipid peroxidation product, was significantly increased upon exposed to 1-BP, which was significantly attenuated by melatonin pretreatment, indicating that administration of 1-BP could interfere with redox homeostasis of brain in rat, and such 1-BP-induced biomedical changes were reversed by treatment with melatonin.

We conclude that treatment with melatonin attenuates 1-BP-induced CNS toxicity through its ROS scavenging effect.

No MeSH data available.


Related in: MedlinePlus