Polychlorinated Biphenyls in Adipose Tissue, Liver, and Brain from Nine Stillborns of Varying Gestational Ages

Abstract

We analyzed polychlorinated biphenyls (PCBs) in s.c. adipose tissue, liver, and brain of nine fetuses who died in utero. Their median (range) gestational ages and birth weights were 34 (17-40) wk and 2050 (162-3225) g. Three fetuses were small for gestational age. The levels of PCB congener nos. 118, 138, 153, and 180, and the sum of these (sigmaPCB), were calculated in terms of tissue total fat content (ng/g fat). The median (range) sigmaPCB (in ng/g fat) amounted to adipose tissue 235 (97-768), liver 198 (67-362), and brain 50 (22-122). Median (range) sigmaPCB levels in liver and brain were 0.8 (0.4-0.9) and 0.2 (0.1-0.3) times, respectively, as high as the sigmaPCB levels in adipose tissue. There were strong relations between sigmaPCB in adipose tissue and sigmaPCB in liver (r=0.98; p < 0.01), and between sigmaPCB in adipose tissue and sigmaPCB in brain (r=0.91; p < 0.01). Adipose tissue, liver, and brain did not show differences in the distribution of congeners 118, 138, 153, and 180, and there was no statistically significant association between tissue PCB levels and gestational age (r varied between 0.22 and 0.47). Median sigmaPCB levels in fetal adipose tissue proved to be comparable with our previously established sigmaPCB levels in mature breast milk of 93 Dutch women (median 414; range 158-969 ng/g of fat). The PCB congeneric distribution of fetal adipose tissue was not different from that of human milk. We conclude that maternal PCBs have a tendency to accumulate notably in fetal tissues with high triglyceride contents. They are easily transferred across the placenta and seem to become equilibrated among the apolar parts of maternal and fetal lipids.

Hippocampal Neurons Exposed to the Environmental Contaminants Methylmercury and Polychlorinated Biphenyls Undergo Cell Death via Parallel Activation of Calpains and Lysosomal Proteases

“…Values are means ± SEM of 8 determinations. Statistical analysis was carried out with the one-way analysis of variance (ANOVA)-Fisher's protected least significant difference (PLSD) test (* P B 0.05, **** P B 0.0001, ## P B 0.01, ### P B 0.001, #### P B 0.0001) concentrations of MeHg (Choi et al 1978) and PCBs (Lanting et al 1998) measured in human brains. However, when comparing the environmental doses with the in vitro doses, one should consider several factors intrinsic to the experimental models, like the cell type (cell line or primary cultures), the confluency of cells, the volume and composition of cell culture media, binding of the chemicals to the plastic walls of culture flasks, and the potential masking properties of serum (Meacham et al 2005).…”

Role of Quercetin on PCBs (Aroclor-1254) Induced Impairment of Dopaminergic Receptor mRNA Expression in Cerebral Cortex of Adult Male Rats

“…PCBs differentially accumulate into microenvironments of living tissues, up to 50 ppb in neonatal human brains [4]. Even a single in vivo PCB exposure of mice reduced the expression of brain dopamine transporter (DAT) and vesicular monoamine transporter (VMAT) proteins [5].…”

The effect of dietary glycine on the hepatic tumor promoting activity of polychlorinated biphenyls (PCBs) in rats

“…PCB-153 is one of the most abundant congeners in the environment, and in both animals and humans (Chu et al 2003;Duarte-Davidson et al 1994;Falandysz et al 1994;Gill et al 2004;Lanting et al 1998;Mariottini et al 2000). Besides being one of the most abundant congeners in the environment, PCB-153 has been previously shown to increase hepatocyte proliferation in rats (Lu et al 2003).…”