A cell facing a metabolite backlog has a limited set of responses, and they divide into two categories: responses that remove or neutralize the offending molecules, and responses that move them somewhere less dangerous. Neither restores the missing catalytic step, so both are damage-limitation strategies.
Detoxification chemically modifies the reactive species so it can no longer attack its targets. Conjugation reactions attach a polar group, such as glutathione, glucuronate, sulfate, or glycine, which both masks the reactive functional group and increases water solubility so the product can be excreted. Reduction and oxidation reactions can also neutralize a reactive group directly. These reactions consume cofactors and reducing equivalents, so sustained detoxification draws on the cell's supply of NADPH and glutathione and can itself become a limiting factor.
Export moves the metabolite out of the compartment or out of the cell. Transporters in the plasma membrane and in organellar membranes pump specific solutes against their gradient, which lowers the internal concentration and relieves osmotic and pH pressure. Export is effective only if the surrounding compartment or the extracellular space can accept the load, so it shifts the problem rather than eliminating it.
Sequestration stores the excess in a physically separated or chemically bound form. The classic example is the storage of excess glucose as glycogen: the polymer is osmotically far less active than the equivalent number of free glucose molecules, so polymerization solves an osmotic problem without destroying the material. Similar logic applies to lipid droplets, protein-bound pools, and vacuolar or lysosomal storage. Sequestration is a buffer, not a solution: the storage capacity is finite, and the stored material can itself become harmful if it accumulates beyond what the storage system can hold, or if it is released back into the cytosol under stress.
Together these responses buy time and limit damage, but the underlying lesion remains. If the block persists, the cell eventually exhausts its detoxification capacity, its export capacity, or its storage capacity, and the damage routes described earlier resume.