Cadmium (Cd) is a persistent environmental toxicant associated with neurological injury, but the role of mitophagy remains unresolved because increased pathway markers may indicate protective clearance, broad mitochondrial selection or incomplete downstream degradation. This review evaluates mitochondrial quality-control checkpoints in Cd-exposed neural systems, focusing on PINK1-Parkin, BNIP3L/NIX and autophagy-lysosome completion, and examines intervention evidence from puerarin, daidzein and ginsenoside Rg1. Three states are proposed as a conceptual synthesis: adaptive clearance, candidate disproportionate mitochondrial elimination and initiated but stalled flux. Protective PINK1- and BNIP3L-dependent activity has loss-of-function support, whereas selection-pathway engagement accompanied by mitochondrial loss is consistent with, but does not establish, disproportionate elimination because degradation and replacement have not been measured together. Cd also disrupts trafficking, autophagosome-lysosome fusion, lysosomal integrity and proteolysis, providing stronger evidence for incomplete bulk autophagic processing than for mitochondria-specific stalled flux. Among the compounds examined, puerarin has the broadest checkpoint coverage, largely from related cortical studies, linking reduced Cd burden and mitochondrial stress with pool preservation and improved bulk autophagic processing. Evidence for daidzein remains marker-limited, whereas Rg1 protects neuronal and glial endpoints without an established Cd-specific mitochondrial quality-control mechanism. This narrative, non-systematic synthesis is limited by potential selection bias, reliance on static markers, dominance of acute or high-dose exposure models, limited measurement of mitochondria-specific degradation and replacement, inadequate cell-type resolution and scarce independent replication. Resolving these states requires mitochondria-specific flux reporters, direct degradation and replacement indices, causal pathway perturbation and matched Cd and compound exposure. Therapeutic benefit is more likely to arise from restoring selective, proportionate and completed mitochondrial turnover balanced by replacement than from uniformly activating or suppressing mitophagy.
