Nickel chloride inhibited the growth of 3T3 mouse fibroblasts in cultu
re within 72 hr at 100 mu M. This cytostatic effect was not accompanie
d by a loss in cell viability as judged by leakage of lactate dehydrog
enase into the culture medium. In the log phase of growth the inhibito
ry effect of 500 mu M nickel chloride was evident within 4hr of exposu
re. This was not accompanied by an alteration in cellular reduced glut
athione content, indicating that oxidative stress was not occurring in
the cells. Inclusion of 100 nM alpha-tocopherol in the culture medium
prevented the cytostatic effect of nickel. Pretreatment with 500 mu M
nickel chloride for 72 hr did not alter glutathione reductase of pero
xidase activities. Nicker has been implicated in the toxic reactions o
ccurring in connective tissue following its use in orthopaedic implant
s. This study shows that the metal inhibits cell growth and may thus d
epress the ingrowth of connective tissue in vivo around the site of im
plant. Furthermore, alpha-tocopherol (vitamin E) may be valuable in pr
eventing some of the problems arising from poorly fitted or loose impl
ants in vivo.