Male infertility can be caused by environmental factors, genetic defects, physiological and endocrine deficiencies and testicular pathologies. Aluminium (Al) can cause male infertility through a number of mechanisms. The aim of our study was thus to determine whether vitamin E (VitE) has protective effects on Al-induced testicular damage, which was determined according to sperm counts and morphology and using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Thirty-four male Wistar rats (250–300 g) were randomly assigned to control (no procedures performed; n = 6) or 0.2 mL intraperitoneal injection group (n = 7 each; three times per week for 4 weeks): sham (distilled water), 10 mg/kg Al, 500 mg/kg VitE and 10 mg/kg Al plus 500 mg/kg VitE (Al + VitE). Sperm samples were evaluated for andrological parameters. The testes were examined by haematoxylin/eosin. The epithelial thickness and areas were calculated and Johnsen scores were determined for the germinal epithelium; the apoptotic indices were determined from TUNEL staining. For Al, the bonds between the germinal epithelial cells were broken in some tubules, and there were unidentified cells in the lumen of some tubules. For control, sham and VitE, normal morphology of the germinal epithelium was generally preserved. With Al + VitE, the full germinal epithelium cell series was maintained, with only mature sperm in the lumen. TUNEL-positive cells were significantly higher with Al compared to control and sham (p < 0.05). For Al + VitE, the number of apoptotic cells was reduced compared to Al alone and was therefore similar to control, sham and VitE (p > 0.05). Our findings show that Al caused testicular damage. VitE reduced the number of apoptotic cells during the damage caused by Al.