The current research was constructed to throw the light on the protective possibility of Chlorella vulgaris (C. vulgaris) and Spirulina platensis (S. platensis) versus lead acetate-prompted testicular dysfunction in male rats. Forty rats were classi ed into four groups; i) control, ii) rats received Lead acetate (30 mg/kg bw), iii) rats were concomitantly received Lead acetate and C. vulgaris (300 mg/Kg bw), vi) rats were simultaneously treated with Lead acetate and S. platensis (300 mg/Kg bw) via oral gavage for 8 weeks. Lead acetate promoted testicular injury as expressed with fall in reproductive organ weights, and gonadosomatic index (GSI). Spermatogenesis disruption is indicated by Sperm cell count reduction, and increased sperm malformation percentage. Steroidogenesis deterioration is evoked by minimized serum testosterone along with maximized follicle-stimulating hormone (FSH), luteinizing hormone (LH) levels. Testicular oxidative, in ammatory, and apoptotic cascades are revealed by elevated Acid phosphatase (ACP) and Sorbitol Dehydrogenase (SDH) serum leakage, declined testicular total antioxidative capacity (TAC) with elevated total oxidative capacity (TOC), tumor necrosis factor alpha (TNF-α), Caspase-3 levels, lessened androgen receptor (AR) expression, and histopathological lesions versus control. Our research highlights that C. vulgaris or S. platensis therapy can modulate lead acetate-promoted testicular dysfunction via antioxidant, immunomodulatory, anti-apoptotic potentials promoted testicular histoarchitecture, and androgen receptor restoration with better impacts to S. platensis comparing to C. vulgaris.