Effects of a Technical PCB Preparation and Fractions Thereof on Ethoxyresorufin O‐Deethylase Activity, Vitamin A Levels and Thymic Development in the Mink (Mustela vison)*

Abstract

Clophen A50, a technical preparation of polychlorinated biphenyls (PCBs), was separated into four fractions; three containing chlorobiphenyls with 0, 1, or 2 to 4 ortho chlorines and one containing di- and tricyclic impurities such as naphthalenes and dibenzofurans. Clophen A50, the four fractions, and a synthetic mixture of the biologically most active non-ortho-chlorinated congeners (3,3',4,4'-tetra-, 3,3',4,4',5-penta-, and 3,3',4,4',5,5'-hexachlorobiphenyl), were separately mixed in the feed and given to female mink during the reproductive season. The concentration of a given compound in the feed mixture was equivalent to its concentration in the feed mixed with Clophen A50. Hepatic 7-ethoxyresorufin O-deethylase (EROD) activity in adults was enhanced 2-3 times by Clophen A50, the fractions containing non- or mono-ortho-chlorinated congeners, and the synthetic mixture. In neonatal kits delivered by females treated with non- or mono-ortho-chlorinated congeners, EROD was enhanced to about 30 times the control value. No live kits were delivered by the females treated with unfractionated Clophen A50. The fractions containing congeners with two to four ortho chlorines or di- and tricyclic compounds did not significantly induce EROD in either adults or kits. Clophen A50 reduced hepatic and pulmonary vitamin A contents in adult mink, while renal vitamin A was unaffected. Responses to the fractions containing the non- and mono-ortho-chlorinated congeners were similar to those obtained with Clophen A50. Their effects were, however, less pronounced, particularly with respect to the hepatic vitamin A reduction. The fractions containing congeners with two to four ortho chlorines and the di- and tricyclic compounds had no significant effects on tissue vitamin A contents.(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamins A1, A2, and E in minks exposed to polychlorinated biphenyls (Aroclor 1242®) and copper, VIA diet based on freshwater or marine fish

“…Decreased level of hepatic vitamin A 1 is frequently found in rodents after exposure to several PCB congeners [29,30]. The only series of experiments conducted with mink [9,10] showed a decrease in hepatic vitamin A 1 with Clophen A50 (commercial PCB mixture, Bayer, LeVerkusen, Germany) but not after exposure to Aroclor 1254. It has been suggested that enzymatic reactions, such as cytochrome P‐450 mono‐oxygenase functions induced by the PCBs, consume vitamin A [8,12,31].…”

“…As in experiments with rodents, seals, and primates [8], PCBs have been found to disturb the vitamin A metabolism of mink [9,10]. In general, several symptoms of PCB administration (decreased growth, impaired reproduction, decreased integrity of epithelial growth, and depressed immune function) are the same as those found in vitamin A deficiency [5,11,12].…”

Tissue distribution of retinoids in common dolphins Delphinus delphis

“…Exposure of experimental animals, such as rats, mink and otters, to organochlorines leads to depletion of hepatic retinoid levels (Brunström et al 1991, Håkans-son et al 1992, Chu et al 1995, Murk et al 1998, Käkelä et al 1999, 2002, Kelley et al 2000, while those in the kidney generally increase (Brouwer et al 1989a, Jurek et al 1990, Nilsson et al 2000. This indicates that the pollutants mobilize retinoid storage forms, which is followed by an increase in their degradation and renal elimination through the urine (Kelley et al 1998(Kelley et al , 2000.…”

Reproductive toxicity in mink (Mustela vison) chronically exposed to environmentally relevant polychlorinated biphenyl concentrations

“…Frozen pieces (∼ 3 g) of the maternal livers were thawed in ice‐cold buffer (0.15 M KCl in 0.05 M Tris‐HCl, pH 7.5) and homogenized in a Potter‐Elvehjem homogenizer (Kontes Glass, Vineland, NJ, USA). Microsomes were prepared by differential centrifugation as previously described [23]. Ethoxyresorufin‐ O ‐dealkylase (EROD) activity in the microsomal fractions was determined using a slightly modified version of the method presented by Pohl and Fouts [24] as previously described [25].…”