D-ribose-L-cysteine exhibits neuroprotective activity through inhibition of oxido-behavioral dysfunctions and modulated activities of neurotransmitters in the cerebellum of Juvenile mice exposed to ethanol
Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randoml...
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Published in: | Drug and chemical toxicology (New York, N.Y. 1978) Vol. 46; no. 4; pp. 746 - 756 |
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Abstract | Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups (n
= 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, p.o), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, p.o) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum. |
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AbstractList | Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups (n
= 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, p.o), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, p.o) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum. Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups (n = 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, p.o), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, p.o) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum. Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups ( = 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, ), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, ) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum. |
Author | Olajide, Olamide Janet Alabi, Sheriffdeen Oluwabusayo Adekomi, Damilare Adedayo Falana, Benedict Abiola Ojo, Waliu Adetunji Adeniyi, Temidayo Daniel Adegoke, Adebiyi Aderinola Adewale, Omowumi Oyeronke Okesina, Akeem Ayodeji Fatoki, John Olabode |
Author_xml | – sequence: 1 givenname: Damilare Adedayo surname: Adekomi fullname: Adekomi, Damilare Adedayo organization: Department of Anatomy, Neuroscience and Cell Biology Unit, Osun State University – sequence: 2 givenname: Olamide Janet surname: Olajide fullname: Olajide, Olamide Janet organization: Department of Anatomy, Neuroscience and Cell Biology Unit, Osun State University – sequence: 3 givenname: Omowumi Oyeronke surname: Adewale fullname: Adewale, Omowumi Oyeronke organization: Department of Biochemistry, Faculty of Basic and Applied Sciences, Osun State University – sequence: 4 givenname: Akeem Ayodeji surname: Okesina fullname: Okesina, Akeem Ayodeji organization: Department of Human Anatomy, Kampala University – sequence: 5 givenname: John Olabode surname: Fatoki fullname: Fatoki, John Olabode organization: Department of Medical Biochemistry, Faculty of Basic Medical Sciences, Osun State University – sequence: 6 givenname: Benedict Abiola surname: Falana fullname: Falana, Benedict Abiola organization: Department of Anatomy, Neuroscience and Cell Biology Unit, Osun State University – sequence: 7 givenname: Temidayo Daniel surname: Adeniyi fullname: Adeniyi, Temidayo Daniel organization: Department of Medical Laboratory Science, Faculty of Allied Health Science, University of Medical Sciences – sequence: 8 givenname: Adebiyi Aderinola surname: Adegoke fullname: Adegoke, Adebiyi Aderinola organization: Department of Anatomy, Neuroscience and Cell Biology Unit, Osun State University – sequence: 9 givenname: Waliu Adetunji surname: Ojo fullname: Ojo, Waliu Adetunji organization: Department of Anatomy, Faculty of Basic Medical Sciences, Ladoke Akintola University of Technology – sequence: 10 givenname: Sheriffdeen Oluwabusayo surname: Alabi fullname: Alabi, Sheriffdeen Oluwabusayo organization: Department of Science Laboratory Technology, Federal Polytechnic |
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Snippet | Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate... |
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SubjectTerms | alcohol Animals Antioxidants - metabolism Antioxidants - pharmacology Catalase - metabolism Cerebellar Diseases - metabolism Cerebellum - metabolism dopamine Dopamine - metabolism Ethanol - toxicity Glutathione Peroxidase - metabolism Lipid Peroxidation Mice Oxidative Stress Purkinje neurons Ribose-cysteine Serotonin Superoxide Dismutase - metabolism |
Title | D-ribose-L-cysteine exhibits neuroprotective activity through inhibition of oxido-behavioral dysfunctions and modulated activities of neurotransmitters in the cerebellum of Juvenile mice exposed to ethanol |
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