Increased reactive oxygen species (ROS) resulting from hyperglycemia and inadequate endogenous antioxidant systems are responsible for the complications of diabetes. ROS accumulate in the cell and stimulate apoptosis, which compromises sperm quality and function. We investigated the possible effects of fucoidan, a potent antioxidant with a regulatory effect on blood glucose homeostasis, on the testicular tissues of rats with experimental diabetes. Diabetes was induced by administering 40 mg/kg streptozotocin (STZ) on five consecutive days. Twenty-four Wistar albino male rats were divided into four groups: group 1, control group (CG); group 2, diabetes group (DG); group 3, early fucoidan group (EFG) treated with 50 mg/kg fucoidan after diabetes induction; group 4, late fucoidan group (LFG) treated with the same dose of fucoidan 15 days after diabetes induction. Fucoidan was administered intraperitoneally every two days for four weeks. Basement membrane thickness and Johnsen scores were higher in the DG than in the CG; no difference was found for either the EFG or LFG compared to the CG. Seminiferous tubule diameters of EFG were significantly greater than for the DG. Apoptotic tubule and apoptotic cell indexes were significantly greater in the DG and significantly less in the EFG and LFG groups compared to the CG. Early use of fucoidan in diabetic individuals may minimize damage to testicular tissue.