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Triethyllead chloride was added directly to male rat liver microsomes (0.0, 0.05, 0.25, 0.5, 1.0, and 3.0 mM), or the rats were pretreated with ip injections, once a day for 2 days (0.0, 1.5, and 3.0 mg triethyllead chloride/kg body wt), and microsomes prepared without any further treatment on Day 3. The effects of these treatments on microsomal N-oxygenation and C-oxygenation in vitro were studied by using N-oxide formation and N-demethylation of N,N-dimethylaniline (DMA) as test reactions. Increased microsomal N-oxygenation was obtained by in vivo treatment and decreased microsomal C-oxygenation by in vitro treatment. As a result, either treatment thus gave rise to an increase in the N-oxygenation/C-oxygenation ratio. Conditions favoring accumulation of the N-oxide product may potentiate the tumor-inducing characteristics of carcinogenic aromatic amines.

Female mice were treated with triethyl lead chloride orally on Days 3–5 after mating. Decreased frequencies of pregnancy were observed at doses of 3.0 (p < 0.0005) and 2.2 mg/kg body wt (p < 0.025). Animals given 1.5 mg/kg showed a decreased frequency of implanted ova (p < 0.0005). No effects upon the percentage of viable embryos were observed at doses of 0.5 and 1.5 mg/kg.

Triethyl lead chloride (TEL) was added directly to female rat liver microsomal fractions at final concentrations of 0.0, 0.005, 0.05 and 0.5 mM, respectively. The effect of oestradiol on liver microsomal metabolism was studied in vitro by incubating the microsomes with radioactive oestradiol-17 beta. The oestradiol metabolites were separated, identified and quantified. The highest treatment concentrations resulted in decreased activities of enzymes that metabolize oestradiol-17 beta.

Female mice were injected intraperitoneally daily from day 18 of gestation and throughout lactation with triethyl lead chloride (TEL; 0.0, 0.5 and 1.0 mg/kg body wt). Off-spring of treated mothers displayed a slight perinatal growth retardation. Male off-spring appeared to be more sensitive to TEL, as indicated by their lower body weights. During the latter half of the lactation period the treated sucklings grew faster than controls, thereby compensating for their initially retarded growth, by the time of weaning. The hepatic cytochrome P-450 content of 9 to 10-day old sucklings of treated mothers was lower than in corresponding controls. We suggest that perinatal growth retardation is initiated by a disturbance in the uterus, e.g. reduced nutrient transport across the placenta.

In order to study the effect of organolead on the placental transfer of amino acids, triethyl lead chloride was administered by i.p. injections to pregnant guinea-pigs. The following day, the fetal part of the placenta was perfused in situ during i.v. infusion of α-aminoisobutyric acid (AIB) to the dam. It was found that triethyl lead treatment (2.5 mg/kg body wt) decreased the AIB-concentration in perfusion media compared with that of the control group. Treatment with 1 mg/kg body wt has no effect. It was also shown that the placental uptake of AIB in animals receiving 2.5 mg/kg body wt is significantly reduced compared with that of the control group. No such effect was obtained in animals receiving 1 mg/kg body wt. It is suggested that triethyl lead may inhibit placental Na+-K+-adenosinetriphosphatase, an enzyme involved with placental amino acid transport. Another possible explanation is a reduction in maternal placental blood flow.

Female mice were injected intraperitoneally with triethyl lead chloride (3.0 or 6.0 mg/kg body weight, respectively) once a day on days 3–4 after mating. At the time of blastocyst implantation the plasma level of progesterone was significantly lower in females given 3.0 mg/kg body weight and the plasma levels of 17β-oestradiol and progesterone were significantly lower in females given 6.0 mg/kg body weight than in control females.