Vitamin A deficiency impairs intestinal physical barrier function of fish.

The present study was the first to investigate the effects of dietary vitamin A (VA) on the intestinal physical barrier function associated with oxidation, antioxidant system, apoptosis and cell-cellular tight junction (TJ) in the proximal (PI), mid (MI) and distal (DI) intestines of young grass carp (Ctenopharyngodon idella). Fish were fed graded levels of dietary VA for 10 weeks, and then a challenge test using an injection of Aeromonas hydrophila was conducted for 14 days. Results indicated that dietary VA deficiency caused oxidative damage to fish intestine partly by the reduced non-enzymatic antioxidant components glutathione (GSH) and VA contents as well as reduced antioxidant enzyme activities [not including manganese superoxide dismutase (MnSOD)]. Further results observed that the decreased antioxidant enzyme activities by VA deficiency were partly related to the down-regulation of their corresponding mRNA levels which were regulated by the down-regulation of NF-E2-related factor 2 (Nrf2) mRNA levels and up-regulation of kelch-like-ECH-associated protein (Keap1a) (rather than Keap1b) mRNA levels in three intestinal segments of fish. Meanwhile, VA deficiency up-regulated the mRNA levels of the apoptosis signalling [caspase-3, caspase-8, caspase-9 (rather than caspase-7)] associated with the inhibition of the target of rapamycin (TOR) signalling pathway in three intestinal segments of fish. Additionally, VA deficiency decreased the mRNA levels of TJ complexes [claudin-b, claudin-c, claudin-3, claudin-12, claudin-15a, occludin and zonula occludens-1 (ZO-1) in the PI, MI and DI, as well as claudin-7 and claudin-11a in the MI and DI] linked to the up-regulation of myosin light chain kinase (MLCK) signalling. These results suggested that VA deficiency impaired structural integrity in three intestinal segments of fish. Meanwhile, excessive VA also showed similar negative effects on these indexes. Taken together, the current study firstly demonstrated that VA deficiency impaired physical barrier functions associated with impaired antioxidant capacity, aggravated cell apoptosis and disrupted TJ complexes in the PI, MI and DI, but different segments performed different actions in fish. Based on protecting fish against protein oxidation, the optimal VA levels for grass carp were estimated to be 2622 IU/kg diet.

SUSPECTED HYPOVITAMINOSIS A-ASSOCIATED SALT GLAND ADENITIS IN NORTHERN ROCKHOPPER PENGUINS ( EUDYPTES MOSELEYI).

Supraorbital salt-excreting glands are present in at least 10 avian orders and are largest in marine species, including penguins. Diseases of the avian salt gland have been described infrequently. From September 2015, five captive northern rockhopper penguins ( Eudyptes moseleyi) were presented over a 6-wk period for unilateral or bilateral supraorbital swellings. In September 2016, two cases recurred and two additional cases were identified. Histopathology demonstrated salt gland adenitis with extensive squamous metaplasia. Blood plasma testing demonstrated marked vitamin A and E deficiencies within the colony. Prolonged frozen storage of feed-fish was implicated as a cause of vitamin depletion; reducing storage times and addition of dietary supplementation prevented recurrence.

Disease manifestations of canine distemper virus infection in ferrets are modulated by vitamin A status.

The measles virus (MV) causes half a million childhood deaths annually. Vitamin A supplements significantly reduce measles-associated mortality and morbidity. The mechanisms whereby vitamin A acts against MV are not understood and currently there is no satisfactory small animal model for MV infection. We report on the development of a ferret model to study antiviral activity of vitamin A against canine distemper virus (CDV). CDV is closely related to MV at the molecular level and distemper in ferrets mimics measles in humans. We infected vitamin A-replete (control) and vitamin A-depleted ferrets with CDV and assessed the ability of high-dose vitamin A supplements to influence CDV disease. In control ferrets, CDV infection caused fever, rash, conjunctivitis, cough, coryza, and diarrhea. In contrast, control ferrets that were given 30 mg of vitamin A did not develop typical distemper after infection and exhibited only a mild rash. The supplement did not negatively affect ferret health and resulted in a 100% increase in serum and liver vitamin A concentrations. We also found that profound vitamin A deficiency is inducible in ferrets and can be rapidly reversed upon high-dose vitamin A supplementation. Vitamin A deficiency caused anorexia, diarrhea, cataracts, behavioral abnormalities, and ultimately death, with or without CDV infection. All ferrets that received vitamin A supplements, however, recovered uneventfully from CDV infection. These results replicate many aspects of the observations of vitamin A therapy in humans with measles and suggest that CDV infection in ferrets is an appropriate model for the study of the antiviral mechanism of vitamin A.