How does environmental pH modulate the toxicity of organic acids to microbial cells in culture?

Introduction / Context:
Organic acids such as acetic, lactic, and benzoic acids are common inhibitors and preservatives. Their inhibitory potency depends strongly on extracellular pH due to acid dissociation equilibria and membrane transport properties.

Given Data / Assumptions:

• Weak acid HA with pKa in the physiological range.
• Cell membrane is relatively permeable to undissociated HA but not to A^-.
• Cytoplasm is buffered near neutral pH.

Concept / Approach:
At lower pH, the fraction of acid in the undissociated form (HA) increases per Henderson–Hasselbalch. HA diffuses across the membrane, dissociates inside the cytosol, and releases protons, collapsing proton motive force and imposing an ATP burden for pH homeostasis. Accumulated anions can also perturb metabolism, elevating toxicity.

Step-by-Step Solution:
Decrease extracellular pH → higher [HA]/[A^-] outside.More HA diffuses inward across lipid bilayer.Inside, HA → H^+ + A^- raising proton load and anion accumulation.Energy diverted to proton pumping and stress responses → inhibited growth.

Verification / Alternative check:
Minimal inhibitory concentrations of weak acids drop as pH is lowered; preservative efficacy of benzoate and sorbate increases at acidic pH, consistent with the mechanism.

Why Other Options Are Wrong:
Decreasing toxicity at low pH contradicts undissociated-acid entry mechanism.pH independence is false for weak acids near their pKa.Fixed maximum at pH 7.0 lacks mechanistic basis.

Common Pitfalls:
Ignoring intracellular buffering limits; assuming charged species cross membranes readily; overlooking energy costs of pH homeostasis.

Final Answer:
Toxicity increases as the pH falls (more undissociated acid penetrates)