Silymarin (SM), an extract from the Silybum marianum (milk thistle) plant containing various flavonolignans (with silybin being the major one), has received a tremendous amount of attention over the last decade as a herbal remedy for liver treatment. In many cases, the antioxidant properties of SM are considered to be responsible for its protective actions. Possible antioxidant mechanisms of SM are evaluated in this review. (1) Direct scavenging free radicals and chelating free Fe and Cu are mainly effective in the gut. (2) Preventing free radical formation by inhibiting specific ROS-producing enzymes, or improving an integrity of mitochondria in stress conditions, are of great importance. (3) Maintaining an optimal redox balance in the cell by activating a range of antioxidant enzymes and non-enzymatic antioxidants, mainly via Nrf2 activation is probably the main driving force of antioxidant (AO) action of SM. (4) Decreasing inflammatory responses by inhibiting NF-κB pathways is an emerging mechanism of SM protective effects in liver toxicity and various liver diseases. (5) Activating vitagenes, responsible for synthesis of protective molecules, including heat shock proteins (HSPs), thioredoxin and sirtuins and providing additional protection in stress conditions deserves more attention. (6) Affecting the microenvironment of the gut, including SM-bacteria interactions, awaits future investigations. (7) In animal nutrition and disease prevention strategy, SM alone, or in combination with other hepatho-active compounds (carnitine, betaine, vitamin B₁₂, etc.), might have similar hepatoprotective effects as described in human nutrition.

Poultry in commercial settings are exposed to a range of stressors. A growing body of information clearly indicates that excess ROS/RNS production and oxidative stress are major detrimental consequences of the most common commercial stressors in poultry production. During evolution, antioxidant defence systems were developed in poultry to survive in an oxygenated atmosphere. They include a complex network of internally synthesised (e.g., antioxidant enzymes, (glutathione) GSH, (coenzyme Q) CoQ) and externally supplied (vitamin E, carotenoids, etc.) antioxidants. In fact, all antioxidants in the body work cooperatively as a team to maintain optimal redox balance in the cell/body. This balance is a key element in providing the necessary conditions for cell signalling, a vital process for regulation of the expression of various genes, stress adaptation and homeostasis maintenance in the body. Since ROS/RNS are considered to be important signalling molecules, their concentration is strictly regulated by the antioxidant defence network in conjunction with various transcription factors and vitagenes. In fact, activation of vitagenes via such transcription factors as Nrf2 leads to an additional synthesis of an array of protective molecules which can deal with increased ROS/RNS production. Therefore, it is a challenging task to develop a system of optimal antioxidant supplementation to help growing/productive birds maintain effective antioxidant defences and redox balance in the body. On the one hand, antioxidants, such as vitamin E, or minerals (e.g., Se, Mn, Cu and Zn) are a compulsory part of the commercial pre-mixes for poultry, and, in most cases, are adequate to meet the physiological requirements in these elements. On the other hand, due to the aforementioned commercially relevant stressors, there is a need for additional support for the antioxidant system in poultry. This new direction in improving antioxidant defences for poultry in stress conditions is related to an opportunity to activate a range of vitagenes (via Nrf2-related mechanisms: superoxide dismutase, SOD; heme oxygenase-1, HO-1; GSH and thioredoxin, or other mechanisms: Heat shock protein (HSP)/heat shock factor (HSP), sirtuins, etc.) to maximise internal AO protection and redox balance maintenance. Therefore, the development of vitagene-regulating nutritional supplements is on the agenda of many commercial companies worldwide.

One hypothesis for why females in many animal species frequently prefer to mate with the most elaborately ornamented males predicts that availability of carotenoid pigments is a potentially limiting factor for both ornament expression and immune function. An implicit assumption of this hypothesis is that males that can afford to produce more elaborate carotenoid-dependent displays must be healthier individuals with superior immunocompetence. However, whether variation in circulating carotenoid levels causes variation in both immune function and sexual attractiveness has not been determined in any species. In this study, we show that manipulation of dietary carotenoid supply invokes parallel changes in cell-mediated immune function and sexual attractiveness in male zebra finches ( Taeniopygia guttata ).

Egg quality is a phenotype of, and can profoundly influence fitness in, both mother and offspring. However, the physiological mechanisms that underlie this maternal effect are poorly understood. Carotenoids are hypothesized to enhance antioxidant activity and immune function, and are responsible for the pigmentation of egg yolk. The proximate basis and consequences of this maternal investment, however, have not previously been studied in wild birds. In this supplemental feeding study of lesser black-backed gulls, Larus fuscus, carotenoid-fed females are shown to have increased integument pigmentation, higher plasma concentrations of carotenoids and antioxidant activity, and lower plasma concentrations of immunoglobulins (Igs) in comparison with controls. In turn, carotenoid-fed females produced eggs containing high carotenoid but low Ig concentrations (i.e. passive immunity), whereas control females produced eggs containing low carotenoid but high Ig concentrations. Within-clutch patterns of these resources varied over the laying sequence in a similar manner in both carotenoid-fed and control nests. Our results suggest that carotenoids could be one resource responsible for egg quality maternal effects in birds. We discuss the possible implications of carotenoid-mediated effects on phenotype for fitness in mothers and their offspring.

1. The effects of selenium and vitamin E supplementation of the maternal diet on their transfer to the egg yolk and tissues of the newly hatched chick and on the development of the antioxidant system in the chick liver in early postnatal life were investigated. 2. One hundred Cobb broiler breeder hens were divided into 10 equal groups and housed in pens at 25 weeks of age. Each hen received 1 of the treatment diets which included 0.2 or 0.4 mg/kg selenium, 40, 100, 200 mg/kg vitamin E or their combination. After 6 weeks, the hens were artificially inseminated once per week. From week 8, eggs were collected and placed in an incubator. After hatching, chicks from each group were reared (under standard commercial conditions) to 10 d of age. The chicks were fed on a standard starter commercial broiler diet. At the time of hatching, and at 5 and 10 days old, 4 chicks from each group were sacrificed and blood, liver and brain were collected for the subsequent biochemical analyses. 3. The inclusion of organic selenium or vitamin E in the commercial diet significantly increased their concentration in the egg and in the liver of 1-d-old chicks obtained from the eggs enriched with these substances. A positive effect of such dietary supplementation was seen at d 5 and d 10 of postnatal development. 4. There was a positive effect of selenium supplementation of the maternal diet on glutathione concentration in the liver of 1-d-old and 5-d-old chicks. A combination of a dietary selenium supplementation with high vitamin E doses further increased glutathione concentration in the liver. Dietary selenium supplementation significantly increased selenium-dependent glutathione peroxidase (Se-GSH-Px) activity in the liver of the 1-d-old and 5-d-old chicks and decreased liver susceptibility to peroxidation. 6. It is concluded that the nutritional status of the laying hen determines the efficiency of the antioxidant system throughout embryonic and early postnatal development of the offspring.