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Sulfur Assimilation

Sulfur Assimilation

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 become...

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Related Experiment Video

Updated: Jul 15, 2026

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds

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Published on: August 25, 2013

Sphinganine-induced lysosomal membrane permeabilization: Interplay with subcellular oxidative levels.

Guodong Cheng¹, Changxi Qi², Huiling Xu¹

¹College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, 271018, China.

Biochimica Et Biophysica Acta. Molecular and Cell Biology of Lipids

|November 10, 2025

Summary

Sphinganine (SA) causes cell death primarily through lysosomal damage, not direct oxidative stress. This finding offers new therapeutic strategies for sphingolipid disorders.

Keywords:

Lysosomal membrane permeabilization Sphinganine Subcellular oxidative levels

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A Pipeline to Investigate the Structures and Signaling Pathways of Sphingosine 1-Phosphate Receptors

A Pipeline to Investigate the Structures and Signaling Pathways of Sphingosine 1-Phosphate Receptors

Published on: June 8, 2022

Area of Science:

Cell Biology
Biochemistry
Toxicology

Background:

Sphinganine (SA) is a key sphingolipid with poorly understood cytotoxicity.
Sphingolipids play crucial roles in cellular functions and diseases.

Purpose of the Study:

To elucidate the precise mechanisms underlying sphinganine-induced cytotoxicity.
To investigate the roles of reactive oxygen species (ROS) and lysosomal integrity in SA toxicity.

Main Methods:

Cellular assays to assess cell death pathways.
Mitochondrial and lysosomal function analysis.
Measurement of hydrogen peroxide levels in cellular compartments.
Inhibition studies using E64D to block cathepsin release.

Main Results:

SA induces cell death predominantly via lysosomal membrane permeabilization (LMP) due to pH and osmotic imbalance.
Mitochondrial ROS contribute to oxidative stress and mitochondrial fragmentation.
Lysosomes colocalize with hydrogen peroxide microdomains, indicating redox-dependent organelle positioning.
Inhibition of cathepsin release by E64D attenuates SA-induced apoptosis, confirming LMP's role.

Conclusions:

SA exhibits a dual organelle toxicity mechanism targeting both mitochondria and lysosomes.
Lysosomal membrane permeabilization is a key executor of SA-induced apoptotic signaling.
Findings provide a therapeutic rationale for treating sphingolipid disorders, including fumonisin B1 toxicity, via lysosomal stabilization or ROS modulation.