Plasma membrane behavior, oxidative damage, and defense mechanism in Phanerochaete chrysosporium under cadmium stress

• Membrane fluidity and H+-ATPase activity were significantly reduced by cadmium.
• Cadmium induced cell death is produced by breakdown of MMP and ROS formation.
• Extracellular cadmium crystal particles were synthesized after exposure to Cd2+.
• Cells survive by activating antioxidant and biosynthesis of crystal particles.

Microorganisms are essential for maintaining ecosystem balance, and understanding their response to toxic pollutants is important in assessing the potential environmental impacts of such releases. In this study, the response to the heavy metal cadmium and the potential defense or adaptive mechanisms of the widely used white-rot fungus, Phanerochaete chrysosporium, were investigated. The results indicated that cadmium causes plasma membrane damage, including rigidification of lipids, a decrease in H+-ATPase activity, and lipid peroxidation. The cellular death may be mediated by oxidative stress with mitochondria membrane potential (MMP) breakdown and reactive oxygen species (ROS) formation. Parts of the cells were able to survive by activating antioxidant defense systems (antioxidant agents and enzymes). Extracellular synthesis of cadmium crystal particles was observed after exposure to dissolved cadmium ion, which is probably another detoxification mechanism in which the dissolved metal is precipitated, thus reducing its bioavailability and toxicity. These physiological responses of P. chrysosporium to cadmium together with the defense mechanisms can provide useful information for the development of fungal-based technologies to reduce the toxic effects of cadmium.