9 

 GA's, such as GA g , GA.q , GA 23 , and GA 24 , exhibited species specificity by 

 being highly active in some bioassays yet induced poor responses in 

 others. A ranking of the overall relative activity, indicated that 

 GA 3 was the most active compound (Stuart and Cathey, 1961; Reeve and 

 Crozier, 1974). Consistently low activity was exhibited by GAg, GA,,, 

 GA 12 , GA 13 , GA U , GA 17 , GA^, GA 25 , GA 27 , GA 28 , GA 29 , GA 33 , and GA 34 . 

 In all bioassay systems, GA 26 was inactive at all concentrations 

 tested. Barendse (1974) indicated that many of the weaker gibberellins 

 were isolated from immature seeds, and it is not certain if (1) they are 

 also present in the growing plant, or (2) they are merely by-products 

 or intermediates for interconversion during biosynthesis of 

 more active gibberellins. 



Toxicology 



Gibberellic acid has been evaluated for toxicological effects in 

 rats, mice, guinea pigs, rabbits, dogs, cats, and chickens (Peck et al . , 

 1957; Warden and Schaible, 1958; Kimura et al . , 1959). The compound was 

 shown to be asymtomatic and free of pathologic changes in subacute toxi- 

 city studies in mice and subchronic toxicity studies in dogs and rats 

 ('Kimura et al . , 1959). Subacute studies showed gibberellic acid to be 

 tolerated by mice at 2 g/kg, intravenously for 5 days, and at 

 1 g/kg, subcutaneously for 14 days (Abbott Laboratories, 1962). Studies 

 of acute intravenous toxicity of gibberellic acid in mice yielded an 

 LD Q of 4.2 g/kg, an LD 5Q of 6.3 g/kg, and an LD 1Q0 of 8.7 g/kg (Peck et 

 al., 1957). Peck et al . (1957) indicated that signs of toxicity were 

 nonspecific and no deaths and only minimal signs of toxicity were 

 observed after the oral administration of 25.0 g/kg to mice. Based on 



