Polychlorobiphenyl toxicity and nutrition. II. PCB toxicity and vitamin A (2).

Abstract

An attempt was made to elucidate the interaction between PCB toxicity and vitamin A. The effects of vitamin A addition or vitamin A deficiency in altering the toxicity of dietary PCB were examined. Rats fed a 0.1 PCB diet supplemented with 3,400 IU of vitamin A for 6 weeks showed better growth than those fed a 0.1% PCB diet only. However, rats given a vitamin A deficient diet with 0.1% PCB showed a significant growth retardation than those given a 0.1% PCB diet only. All rats which were fed a vitamin A deficient diet with PCB closed their eyes 50% or entirely in the last period of the experiment, but such sym ptom was not seen in the rats given a 0.1% PCB diet only or a vitamin A deficient diet. Vitamin A content in the liver decreased significantly with 0.1% PCB administration. It was found that a larger supply of dietary vitamin A than the level contained in the basal diet is required to prevent, to some extent, the growth retardation by PCB administration and to sustain the same level of vitamin A content in the liver of rats fed the same 0.1% PCB diet as that of basal diet group. It was concluded that animals fed PCB require more vitamin A than usual. This suggests the possibility that vitamin A may play a role in the dntoxication of PCB.

Further studies on the reduction of vitamin a content in the livers of rats given polychlorinated biphenyls.

“…Although the diet intake in the 0.1% PCB diet group was approximately 80% of that in the control group, body weight gain in the PCB group was about one half that in the control group. Elevation of serum phospholipid and liver enlarge ment were also observed in the PCB-fed group, as in the previous study (3). Vitamin A content per gram liver of rats fed the 0.1% PCB diet decreased to al most one-fifth that of the control group in the 2nd week after PCB ingestion began, and remained at a low level until the 8th week, while vitamin A content per gram liver of the control group was constant until the 6th week after feeding started and thereafter increased.…”

Effects of 3,3′,4,4′-tetrachlorobiphenyl on the dynamics of vitamin A in brook trout (Salvelinus fontinalis) and intestinal retinoid concentrations in lake sturgeon (Acipenser fulvescens)

“…Lake trout, Sakvelinus namaycush, injected with the coplanar PCB, 3,3',4,4',5-pentachlorobiphenyl, had dramatically decreased liver stores of vitamin A (Palace and Brown 1994). The biological effects of PCBs in laboratory rodents resemble those seen during vitamin A deficiency (Innami et al 1974;Brouwer and Van Den Berg 1984;Azais et al 1987). In the case of humans where a relatively complete set of observations is available, the major effects common to PCB-furm-dioxin toxicity and vitamin A imbalances include reproductive inhibition, teratogenicity, growth inhibition, body mass loss, various dermal disorders (e.g., hyprkeratosis, chloracne-like condition), immunosuppression, susceptibility to infections, and susceptibility to cancers (Parkinson and Safe 1981;Safe 1984;Kamm et al 1984;Underwood 1984;Spear 1985).…”

Increased retinoic acid metabolism following 3,3′,4,4′,5,5′-hexabromobiphenyl injection

“…These include dichlorodiphenyltt-ichlmoethane (DBT) , polychlorinated biphenyl mixtures (PCB), 2,3,7,8-tetrachlorodiknzo-p-dioxin (TCDD) , and polybrominated biphenyl mixtures (PBB) (Phillips 1963;Villeneuve et al 1971;Thunberg et al 1979;Dajom et al 1983). A majority of the effects of chemical exposure are the recognized symptoms of hypovitaminosis A (Vos 19781, and vitamin A supplementation partially protects against toxicity (Innami et al 1974). Unlike typical nutritional vitamin A deficiency; however, total depletion of liver stores is not a prerequisite to toxic effects, and increased semm retino1 concentrations have been reported in some cases (McConnell et al 1978).…”