Effects of protein-deficient nutrition during rat pregnancy and development on developmental hindlimb crossing due to methylmercury intoxication

Pregnant rats were fed either a control (20% protein) or low (3.5%) protein diet during gestation and lactation. The pups were separated from their mo thers on postnatal day 21, and were given the same diet as their correspond ing mothers. The groups of pups from each diet group were treated on either postnatal day 21 or postnatal day 60 with 7.5 mg methylmercury chloride (M eHgCl) per kg b.w. once daily by gavage for 10 consecutive days, and the de velopment of ataxia (hindlimb crossing) was monitored. The offspring from m others on the protein-deficient diet were found to be more sensitive to MeH g-induced ataxia than those on the protein-sufficient diet. The former accu mulated more mercury in different brain regions than the latter. The rates of protein synthesis in different brain regions of the offspring fed the pr otein-deficient diet were significantly reduced compared with the rates in those fed the protein-sufficient diet. However, MeHg treatment did not sign ificantly modify the rates of such protein synthesis further in protein-def icient rats. Thus, a significantly much higher inhibition of the intrinsic rates of protein synthesis in different brain regions due to severe protein deficiency, as observed in this study, may be partly responsible for the i ncreased susceptibility of developing rats fed a protein-deficient diet to MeHg-induced a taxia, or hindlimb crossing, although other factor(s) might also be involved.