Pathways

Zeaxanthin biosynthesis is a pathway that occurs in the chloroplast by which lycopene becomes zeaxanthin, one of the most common carotenoid alcohols found in nature . The first two reactions are catalyzed by lycopene beta cyclase which uses NAD(P)H as a cofactor to convert lycopene into gamma-carotene and gamma-carotene into beta-carotene. The last two reactions are catalyzed by beta-carotene 3-hydroxylase which uses ferredoxin and Fe2+ as cofactors to convert beta-carotene into beta-cryptoxanthin and beta-cryptoxanthin into zeaxanthin.

Zeaxanthin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Zeaxanthin passes through the liver and is then excreted from the body mainly through the kidney.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Ziconotide, also known as SNX-111, is an N-type calcium channel antagonist used to manage patients with severe chronic pain who cannot tolerate, or who have not responded adequately to other treatments such as intrathecal morphine and systemic analgesics. Ziconotide is a neurotoxic peptide derived from the cone snail Conus magus comprising 25 amino acids with three disulphide bonds. It is used to manage severe chronic pain through the inhibition of N-type calcium channels involved in nociceptive signalling.Ziconotide was granted FDA approval on December 28, 2004 under the brand name Prialt. To date, ziconotide is the only calcium channel blocking peptide approved for use by the FDA. Nociceptive pain signalling is a complex processing pathway involving peripheral nociceptors, primary afferent nerve fibres, and downstream CNS neurons located in the spinal cord such as the dorsal root ganglion. Voltage-gated calcium channels (VGCCs) are important regulatory components of neural signalling, including type-N voltage-gated calcium channels. N-type channel activate lightly myelinated Aδ- and C-fibres, which mediate the release of neurotransmitters substance P, calcitonin gene-related peptide (CGRP), and glutamate. This causes downstream nociceptive neuronal activity and pain perception. Substance P and CGRP both also induce inflammation, further exasperating chronic pain. Ziconotide inhibits Voltage-dependent N-type calcium channels in presynaptic neurons. This prevents calcium from entering the neuron which prevents neurotransmitter release from the dorsal root ganglion as well as other nociceptive neurons. Therefore substance P, CGRP, and glutamate are not released into the synapse and cannot activate the substance P receptors, CGRP receptors, or the N-Methyl-D-aspartic acid receptors on the post-synaptic neuron. This causes hyperpolarization, with a down-stream effect of hyperalgesia, a prevention of pain signalling.

Ziconotide, also known as SNX-111, is an N-type calcium channel antagonist used to manage patients with severe chronic pain who cannot tolerate, or who have not responded adequately to other treatments such as intrathecal morphine and systemic analgesics. Ziconotide is a neurotoxic peptide derived from the cone snail Conus magus comprising 25 amino acids with three disulphide bonds. It is used to manage severe chronic pain through the inhibition of N-type calcium channels involved in nociceptive signalling.Ziconotide was granted FDA approval on December 28, 2004 under the brand name Prialt. To date, ziconotide is the only calcium channel blocking peptide approved for use by the FDA. Nociceptive pain signalling is a complex processing pathway involving peripheral nociceptors, primary afferent nerve fibres, and downstream CNS neurons located in the spinal cord such as the dorsal root ganglion. Voltage-gated calcium channels (VGCCs) are important regulatory components of neural signalling, including type-N voltage-gated calcium channels. N-type channel activate lightly myelinated Aδ- and C-fibres, which mediate the release of neurotransmitters substance P, calcitonin gene-related peptide (CGRP), and glutamate. This causes downstream nociceptive neuronal activity and pain perception. Substance P and CGRP both also induce inflammation, further exasperating chronic pain. Ziconotide inhibits Voltage-dependent N-type calcium channels in presynaptic neurons. This prevents calcium from entering the neuron which prevents neurotransmitter release from the dorsal root ganglion as well as other nociceptive neurons. Therefore substance P, CGRP, and glutamate are not released into the synapse and cannot activate the substance P receptors, CGRP receptors, or the N-Methyl-D-aspartic acid receptors on the post-synaptic neuron. This causes hyperpolarization, with a down-stream effect of hyperalgesia, a prevention of pain signalling.