A lactose-binding lectin (TCL) was purified from the seeds of African walnut, Tetracarpidium conophorum, and acute toxicity studies of the lectin were carried out with Swiss albino male mice. Animals were administered doses of TCL from 500 to 2500 mg kg−1 body weight (b.wt.) orally while intraperitoneally the dose ranged from 10 to 600 mg kg−1 b.wt. Animals were then assessed for organ and body weight changes, mortality, and histopathology. TCL did not cause any observable toxicity via the oral route; however, when administered intraperitoneally, TCL elicited toxicity with an LD50 of 50 mg kg−1 b.wt. Death from intoxication was preceded by convulsion, hypoactivity, salivation, ataxia, and weakness. The animals given lethal doses of the lectin showed profound respiratory depression which was judged to be the primary cause of death. Histopathological analysis indicated that the lungs, liver, and spleen were adversely affected while the kidney and other organs were essentially normal. In all the affected organs, the severity of toxicity was dose-dependent as the effect of the lectin became more pronounced with increase of the dose administered.