Pathways

Carbapenems are one of the five groups of the beta-lactam family of antibiotics and are currently the most important in clinical use in their broad specificity and resistance to B-lactamase enzymes. They contain an unsaturated, five-carbon ring fused to the nitrogen and carbon of the four-carbon β-lactam ring and act well against both Gram-positive and Gram-negative bacteria. This pathway shows the synthesis of several carbapenems in the bacterium Streptomyces cattleya and this is apparent from the fact that carbapenems are produced by Streptomyces. The pathway begins with the conversion of L-glutamate-5-semialdehyde (from L-Glutamic acid) and its cyclized form 1-Pyrroline-5-carboxylic acid along with the co-substrate malonyl-CoA into 2S,5S)-5-carboxymethyl proline. This intermediate is then converted into ((3S,5S)-carbapenam-3-carboxylate via the enzyme putative beta-lactam synthetase which is then epimerized and desaturated by carbapenem synthase to form the main product of this pathway: (5R)-Carbapenem-3-carboxylate. Stemming from this product, carbapenem biosynthesis intermediates 1-6 act as intermediates which lead to the synthesis of several variations of compounds that belong to the carbapenem family: thienamycin, N-acetylthienamycin, MM 4550 (a member of the olivanic acids and is the major carbapenem produced by S. argenteolus). It must be noted that the lack of direct connections between compounds in this illustration of the pathway accounts for the hypotheticality of the gene products in the reactions that connect one intermediate to the next.

CCarbamoyl Phosphate Synthetase Deficiency, also called hyperammonemia due to carbamoyl phosphate synthetase 1 deficiency, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the urea cycle caused by a defective CPS1 gene. The CPS1 gene codes for the protein carbamoyl phosphate synthetase I, which plays a role in the urea cycle. This disorder is characterized by a large accumulation of ammonia in the blood. Symptoms of the disorder include unusual movements, seizures, unusual sleeping or coma. Treatment with citrulline or arginine, which maintains a regular rate of protein creation. It is estimated that carbamoyl phosphate synthetase deficiency affects 1 in 800,000 individuals in Japan.

CCarbamoyl Phosphate Synthetase Deficiency, also called hyperammonemia due to carbamoyl phosphate synthetase 1 deficiency, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the urea cycle caused by a defective CPS1 gene. The CPS1 gene codes for the protein carbamoyl phosphate synthetase I, which plays a role in the urea cycle. This disorder is characterized by a large accumulation of ammonia in the blood. Symptoms of the disorder include unusual movements, seizures, unusual sleeping or coma. Treatment with citrulline or arginine, which maintains a regular rate of protein creation. It is estimated that carbamoyl phosphate synthetase deficiency affects 1 in 800,000 individuals in Japan.

CCarbamoyl Phosphate Synthetase Deficiency, also called hyperammonemia due to carbamoyl phosphate synthetase 1 deficiency, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the urea cycle caused by a defective CPS1 gene. The CPS1 gene codes for the protein carbamoyl phosphate synthetase I, which plays a role in the urea cycle. This disorder is characterized by a large accumulation of ammonia in the blood. Symptoms of the disorder include unusual movements, seizures, unusual sleeping or coma. Treatment with citrulline or arginine, which maintains a regular rate of protein creation. It is estimated that carbamoyl phosphate synthetase deficiency affects 1 in 800,000 individuals in Japan.

Carbamoyl Phosphate Synthetase Deficiency, also called hyperammonemia due to carbamoyl phosphate synthetase 1 deficiency, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the urea cycle caused by a defective CPS1 gene. The CPS1 gene codes for the protein carbamoyl phosphate synthetase I, which plays a role in the urea cycle. This disorder is characterized by a large accumulation of ammonia in the blood. Symptoms of the disorder include unusual movements, seizures, unusual sleeping or coma. Treatment with citrulline or arginine, which maintains a regular rate of protein creation. It is estimated that carbamoyl phosphate synthetase deficiency affects 1 in 800,000 individuals in Japan.

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

Carbamazepine is an oral drug used as an antiepileptic, analgesic and mood stabilizer drug. It is used to treat conditions including simple and complex partial seizures, generalized tonic-clonic seizures, trigeminal neuralgia, acute mania or mixed episodes in bipolar I disorder. Carbamazepine acts in neurons where it inhibits voltage gated sodium channels in the pre synaptic neurons. In neurons, voltage gated sodium channels allow sodium to come into the neuron triggering the depolarization phase. the potassium channels are responsible for the repolarization phase to bring the neuron back to resting potential. The action potentials created travel down the axon of the neuron and at the nerve terminal, calcium channels open, allowing calcium to enter the cell. Calcium entry causes synaptic vesicles containing neurotransmitters like glutamate to fuse with the membrane and expel the neurotransmitter into the synapse. Glutamate binds to AMPA and NMDA receptor on the post synaptic neurons where they cause excitation of the neuron. By blocking the voltage gated sodium channels, carbamazepine prevents the depolarization phase, inhibiting action potential generation and the release of excitatory neurotransmitter like glutamate. Pre and post synaptic neuronal firing are therefore reduced. Carbamazepine works as a “use-dependent” block. This means that it preferentially binds to channels that are being opened. In neurons that are repetitively firing, their sodium channels are being opened more often, and as a result, carbamazepine is able to produce a greater block in these neurons. This property of carbamazepine is essential in treating conditions like seizures, trigeminal neuralgia and mania which caused by excessive neuronal activity. Side effects of carbamazepine include dizziness, drowsiness, ataxia, nausea, vomiting, water retention, hyponatremia, severe bone marrow depression, hypersensitivity reactions and gastrointestinal and cardiovascular dysfunctions.

Carbamazepine is a drug used in the treatment of epilepsy, bipolar disorder, trigeminal neuralgia, and other psychiatric disorders. Carbamazepine is almost entirely metabolized in the liver, with the primary metabolic pathway being conversion to 10,11-epoxycarbamazepine. Ring hydroxylation to 2-hydroxycarbamazepine and 3-hydroxycarbamazepine represent a minor metabolic route, presumably though a carbamazepine 2,3-epoxide intermediate. Potential bioactivation occurs via CYP3A4-mediated secondary oxidation of 2-hydroxycarbamazepine to the potentially reactive carbamazepine iminoquinone and of 3-hydroxycarbamazepine to form other reactive metabolites. Radicals can also be formed from metabolism of 3-hydroxycarbamazepine by myeloperoxidase. Oxcarbazepine, an anticonvulsant used primarily in the treatment of epilepsy, is converted to 10,11-dihydroxycarbamazepine via 10-hydroxycarbazepine.