Related Experiment Video
Updated: Jun 19, 2026

08:09
Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Lycopene modulates nitric oxide pathways against 3-nitropropionic acid-induced neurotoxicity
Puneet Kumar1, Harikesh Kalonia, Anil Kumar
1Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India.
Life Sciences
|October 14, 2009
Summary
Lycopene protects against Huntington
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Huntington's disease is a neurodegenerative disorder.
- 3-nitropropionic acid (3-NP) is used to induce Huntington's disease-like symptoms in rats.
- Lycopene is a potent antioxidant with potential therapeutic benefits.
Purpose of the Study:
- To investigate the role of the nitric oxide (NO) mechanism in lycopene's protective effects against 3-NP-induced Huntington's disease-like symptoms in rats.
Main Methods:
- Rats were treated with 3-NP to induce disease symptoms.
- Lycopene was administered orally at different doses.
- Behavioral, biochemical, and mitochondrial enzyme activities were assessed.
- The involvement of nitric oxide was examined using L-arginine and L-NAME.
Main Results:
- Lycopene treatment significantly attenuated behavioral and biochemical impairments caused by 3-NP.
- Lycopene protected against reduced oxidative defense and impaired mitochondrial enzyme activities.
- Nitric oxide modulation influenced lycopene's protective effects.
Conclusions:
- Nitric oxide modulation plays a role in lycopene's protective effects against 3-NP-induced neurodegeneration.
- Lycopene demonstrates potential as a therapeutic agent for Huntington's disease.
Related Concept Videos
Nitric Oxide Signaling Pathway
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Drugs Affecting Neurotransmitter Synthesis
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Bioactivation and Tissue Toxicity
Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...