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Sulfur Assimilation01:20

Sulfur Assimilation

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Sulfur is an essential element in biological systems, contributing to synthesizing key biomolecules, including amino acids such as cysteine and methionine, and cofactors such as coenzyme A and biotin. Microorganisms primarily assimilate sulfur as sulfate (SO₄²⁻) from the environment, which must undergo a series of biochemical transformations before it can be incorporated into cellular components. As sulfate is highly oxidized, it must undergo assimilatory sulfate reduction to...
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Phase II Reactions: Sulfation and Conjugation with α-Amino Acids01:19

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Sulfation and α-amino acid conjugation are two critical biotransformation reactions in drug metabolism. Sulfation, a phase II biotransformation reaction, involves adding a polar sulfate group to a drug, enhancing its water solubility and promoting excretion. This process can either co-occur with or occur independently of glucuronidation. Nonmicrosomal sulfotransferase enzymes catalyze the process. The reaction involves 3'-phosphoadenosine-5'-phosphosulfate or PAPS coenzyme...
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Sulfides are the sulfur analog of ethers, just as thiols are the sulfur analog of alcohol. Like ethers, sulfides also consist of two hydrocarbon groups bonded to the central sulfur atom. Depending upon the type of groups present, sulfides can be symmetrical or asymmetrical. Symmetrical sulfides can be prepared via an SN2 reaction between 2 equivalents of an alkyl halide and one equivalent of sodium sulfide.
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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
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Drug Metabolism: Phase II Reactions01:14

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Phase II reactions are essential for the detoxification and elimination of drugs from the body. These reactions involve the conjugation of parent drugs or their phase I metabolites with endogenous molecules, resulting in more hydrophilic drug conjugates. The primary conjugation reactions in this phase are sulfation and glucuronidation. Both sulfation and glucuronidation typically produce biologically inactive metabolites. However, in some cases involving prodrugs, active metabolites may be...
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Thiols are prepared using the hydrosulfide anion as a nucleophile in a nucleophilic substitution reaction with alkyl halides. For instance, bromobutane reacts with sodium hydrosulfide to give butanethiol.
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Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
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Sulfation Pathways During Neurodevelopment.

Taylor Clarke1, Francesca E Fernandez1, Paul A Dawson2

  • 1School of Behavioural and Health Sciences, Faculty of Health Sciences, Australian Catholic University, Banyo, QLD, Australia.

Frontiers in Molecular Biosciences
|May 2, 2022
PubMed
Summary
This summary is machine-generated.

Sulfate maintenance genes are crucial for neurological function. This review identifies 18 candidate genes linked to neurological dysfunction, offering insights into sulfate homeostasis and brain development.

Keywords:
brainembryologicalfetalgene expressionneurological dysfunctionsulfate

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Area of Science:

  • Biochemistry
  • Developmental Biology
  • Neuroscience

Background:

  • Sulfate is vital for mammalian physiology, influencing cellular functions.
  • Animal studies link sulfate maintenance genes to neurological issues like seizures and developmental problems.
  • Despite conserved pathways, few sulfate genes are clinically recognized.

Purpose of the Study:

  • To review sulfate maintenance genes' expression in the developing human brain.
  • To identify sulfate genes associated with neurological dysfunction in humans and animals.
  • To highlight candidate genes for future clinical investigation.

Main Methods:

  • Curated temporal and spatial expression of 91 sulfate genes in fetal brains (4-17 weeks postconception).
  • Systematic literature search (PubMed, Embase) for neurological phenotypes linked to sulfate genes.
  • Database search (OMIM) for genetic and phenotypic information.

Main Results:

  • Detailed expression patterns of 91 sulfate maintenance genes in the human fetal brain.
  • Identified sulfate genes associated with neurological phenotypes in human and animal models.
  • Discovered 18 candidate neurological dysfunction genes not currently in clinical use.

Conclusions:

  • This review provides a comprehensive overview of sulfate biology genes.
  • Highlights the potential of 18 candidate genes for understanding neurological conditions.
  • Informs future research on sulfate homeostasis disruptions in neurological disorders.