Sprague‐Dawley rats were injected sc with lead acetate in suspension, or with sodium acetate (controls) on the d 9 of pregnancy and every 3–4 d thereafter until the pups were 13 or 21 d of age. At termination, testicular homogenates or isolated Sertoli cells were used to study steroidogenesis and gonadotropin binding. Lead had no significant effect on the mother's water and food consumption, on the pup's body or testis weights, on the number of pups and the time of birth, and on the seminiferous tubule diameter. Homogenates of testes of the lead‐treated group converted significantly less (p <0.01) labeled progesterone (14Cor3H) to 5α‐pregnane‐3,20‐dione, 3α‐hydroxy‐5α‐pregnan‐20‐onet17β‐hydroxy‐5α‐androstan‐3‐one (DHT), 3(α,β))‐hydroxy‐5α‐androstan‐17‐one, testosterone/17α‐hydroxyprogesterone, and androstenedione. Sertoli cells from lead‐treated animals converted significantly less (p < 0.01) progesterone to 5α‐pregnane‐3α,20α‐diol, 3α‐hydroxy‐5α‐pregnan‐20‐one, DHT, and 20α‐hydroxy‐4‐pregnen‐3‐one. These data and direct spectrophotometric assays indicated that 3α‐hydroxysteroid oxidoreductase (3α‐HSO), 3β‐HSO, 20α‐HSO, Sctreductase, and C17–20‐lyase had been affected. The receptor studies showed that the binding of [125I]rFSH to testicular receptors was significantly reduced from 35,600 (control) to 25,980 cpm/mg protein (lead). This is the first evidence that lead exposure fin utero and via mother's milk) significantly reduces steroid production and hormone binding in the testis at the onset of puberty.