The protective effects of dietary pyrroloquinoline quinone disodium (PQQ.Na2) supplementation against oxidized sunflower oil-induced oxidative stress and liver injury in laying hens were examined. Three hundred and sixty 53-week-old Hy-Line Gray laying hens were randomly allocated into one of the five dietary treatments. The treatments included: (1) a diet containing 2% fresh sunflower oil; (2) a diet containing 2% thermally oxidized sunflower oil; (3) an oxidized sunflower oil diet with 100 mg/kg of added vitamin E; (4) an oxidized sunflower oil diet with 0.08 mg/kg of PQQ.Na2; and (5) an oxidized sunflower oil diet with 0.12 mg/kg of PQQ.Na2. Birds fed the oxidized sunflower oil diet showed a lower feed intake compared to birds fed the fresh oil diet or oxidized oil diet supplemented with vitamin E (P=0.009). Exposure to oxidized sunflower oil increased plasma malondialdehyde (P<0.001), hepatic reactive oxygen species (P<0.05) and carbonyl group levels (P<0.001), but decreased plasma glutathione levels (P=0.006) in laying hens. These unfavorable changes induced by the oxidized sunflower oil diet were modulated by dietary vitamin E or PQQ.Na2 supplementation to levels comparable to the fresh oil group. Dietary supplementation with PQQ.Na2 or vitamin E increased the activities of total superoxide dismutase and glutathione peroxidase in plasma and the liver, when compared with the oxidized sunflower oil group (P<0.05). PQQ.Na2 or vitamin E diminished the oxidized sunflower oil diet induced elevation of liver weight (P=0.026), liver to BW ratio (P=0.001) and plasma activities of alanine aminotransferase (P=0.001) and aspartate aminotransferase (P<0.001) and maintained these indices at the similar levels to the fresh oil diet. Furthermore, oxidized sunflower oil increased hepatic DNA tail length (P<0.05) and tail moment (P<0.05) compared with the fresh oil group. Dietary supplementation of PQQ.Na2 or vitamin E decreased the oxidized oil diet induced DNA tail length and tail moment to the basal levels in fresh oil diet. These results indicate that PQQ.Na2 is a potential antioxidant and is as effective against oxidized oil-related liver injury in laying hens as vitamin E. The protective effects of PQQ.Na2 against liver damage induced by oxidized oil may be partially due to its role in the scavenging of free radicals, inhibiting of lipid peroxidation and enhancing of antioxidant defense systems.

During clinical investigation of a commercial herd it was found that intake of supplemented poultry litter (PL) by beef cows at >10 kg/day, was associated with severe cachexia and a mortality rate of between 10 and 20% of cows. Postmortem analysis of 40 fresh carcasses and elevated serum levels of cholesterol, bilirubin, alkaline phosphatase, glutamic oxaloacetic transaminase and sorbitol dehydrogenase in cachetic cows indicated that the cows suffered severe liver damage. The interrelationship between liver damage and PL intake was subsequently investigated in three groups of 20 beef cows each, consuming 0, 3 and 10 kg PL respectively. As determined by the serum indices, intake of 3 kg PL seemed to be sufficient to cause liver damage, although these cows appeared healthy.

In another experiment, six beef cows were stall-fed a diet giving separate access to PL and wheat straw. PL intakes were 3·1,4·7 and 6·0 kg/day. Ruminal ammonia concentration was three to five times higher than the estimate of that required for maximal fermentation in the rumen. The high pH values (6·81 to 6·97) found are optimal for absorption of ammonia from the rumen. The combination of excess absorption of ammonia from the gut and low metabolizable energy intake might have been the cause of liver damage.