Background/Objectives: Dietary mineral deficiencies rarely occur singly, yet most experimental work on the testis has used single-nutrient designs and endpoints, such as sperm number, that cannot tell where spermatogenesis fails. We asked whether isolated deficiency of magnesium, iron, selenium and zinc interrupts spermatogenesis at different stages and whether combined deficiency exceeds the effect of any single element. Methods: Outbred male rats were fed certified purified diets on a common base for twelve weeks from the age of three months: control, magnesium-, iron-, selenium-, zinc- and combined-deficient (six groups, n = 15 each). Testes were examined at six months by morphometry, a stage-resolved census of germ cells per tubule profile with three transition ratios, Johnsen scoring, van Gieson histochemistry and imprint cytology. Results: Every deficiency thinned the spermatogenic epithelium and reduced luminal spermatozoa, but the step affected differed. Selenium restriction lowered the spermatid-to-spermatocyte ratio to 4.05 against 4.98 in controls while sparing the adjacent transitions, a block at meiotic exit. Zinc restriction left that ratio unchanged (5.00) but reduced the spermatozoa-to-spermatid ratio to 1.45 against 1.68, a post-meiotic block, and spared spermatogonia. Magnesium and iron restriction suppressed all germ cell classes in proportion. Combined deficiency lowered two transitions at once and produced the steepest losses: spermatids fell 40.4%, the Johnsen score fell from 10 to 7.4 and Leydig cell density fell 24.5%, against at most 9.0% for any single element. Conclusions: The four deficiencies leave distinguishable structural signatures that sperm number alone does not reveal. Combined deficiency exceeds every single element, markedly so in the Leydig cell compartment, which argues for correcting concurrent deficiencies together rather than one at a time.