Biofuel co-products as livestock feed - Opportunities and challenges

106Biofuel co-products as livestock feed – Opportunities and challengesIn a classical demonstration of this process, Dougherty,Mullenax and Allison, 1965 infused H 2 S into the rumenof sheep and reported that sheep with an open tracheacollapsed after several eructations, whereas sheep with ablocked trachea produced no clinical signs of S toxicosis. Assuch, Bird (1972) stated that “the direct and shorter routeto the heart and brain is afforded by the inspiration of H 2 Sand transfer into the pulmonary vein, which effectively bypassesthe liver and enables H 2 S to exert its toxic effect onthe respiratory-circulatory systems.”Manifestation of S toxicityOn the basis of other gas sensors and gas-based signallingpathways, metallo proteins, particularly haem-containingproteins serve as target molecules and probably mediateeffects of H 2 S. Because of its small size relative to otherthiols, H 2 S has easy access to the metal centres of metalloproteins.The H 2 S may ligate reversibly to the ferric ionof haem. At higher concentrations (e.g. 20 µM), the H 2 Sreduces the ferric ion to ferrous and becomes oxidizedto persulphide (HS-SH). Above-normal concentrationsof H 2 S favour production of sulphhaemoglobin andsulphmyoglobin, both of which have lesser abilities to carryO 2 than haemoglobin. High concentrations of H 2 S alsoreduce methaemoglobin (Pietri, Roman-Morales and Lopez-Garriga, 2010).Sulphide inhibits the functions of carbonic anhydrase,dopa oxidases, catalases, peroxidases, dehydrogenases anddipeptidases, thus affecting oxidative metabolism and theproduction of ATP (Short and Edwards, 1989). Specifically,H 2 S is also thought to block the enzyme cytochrome coxidase (Collman et al., 2009). Blockage of oxidative processesbecomes particularly evident in the brain because ofthe numerous oxidative processes, low concentrations ofantioxidants and the inability of the brain to repair itself(Olkowski et al., 1992). At submicromolar concentrations,H 2 S seems to have a protective effect in nervous tissuebecause it can protect neurons against hypoxic injury, inhibitoxidative damage, increase glutathione production, scavengereactive oxygen species and suppress mitochondrialoxidative stress (Bouillaud and Blachier, 2011). In fact, deficiencyof H 2 S production may be associated with Alzheimer’sdisease in humans. At high concentrations, H 2 S decreasescellular respiration and can substantially limit the amount ofO 2 delivered to the brain and the rate of ATP generation inthe brain. Such a severe restriction in ATP generation in thebrain causes necrosis of the cerebral cortex and softeningof the brain tissue (Gould, 1998). Mild cases of H 2 S toxicityin ruminants do not always, but can, result in decreasedDM intake and average daily gain. Manifestations of S toxicosisinclude anorexia, weight loss, constipation, diarrhoeaand depression. Severe cases of H 2 S toxicity may result inPEM (Gould, 1998). Polioencephalomalacia literally meanssoftening (malacia) of the gray matter (polio) of the brain(encephalo). Signs of PEM include separation from thegroup, head pressing, “star gazing” in which cattle standwith their head held back and upward, teeth grinding andhave a staggered gait. More extreme and advanced signsmay include seizures, blindness and coma, and may eventuallylead to death.In the cardiovascular system, H 2 S apparently exertsvasodilation and vasoconstriction effects depending on oxygenconcentrations and interaction with other gasotransmitterssuch as NO (Leschelle et al., 2005). At low concentrations,H 2 S can positively decrease blood pressure(Olson, 2011), however, at toxic concentrations, H 2 S hasa paralyzing effect on the carotid body, further inhibitingnormal respiration (Bulgin, Stuart and Mather, 1996).Thus, elevated pulmonary arterial pressure with increasingS intake has been observed (Loneragan et al., 1998) andothers (Bulgin, Stuart and Mather, 1996; Coghlin, 1944)have noted pulmonary oedema and respiratory distress as afeature of H 2 S poisoning. Because H 2 S is so toxic (Truong etal., 2006), damage to lung tissue could result even if clinicalsigns of PEM do not exist. Decreases in intake and gainhave been reported for cattle fed diets containing as littleas 0.22 percent S (Zinn et al., 1997, 1999), and continuedlinear decreases have been observed up to 0.46 percent Sby numerous authors (Bolsen, Woods and Klopfenstein,1973; Loneragan et al., 2001; Spears and Lloyd, 2005).Potential mechanisms of S toxicity in ruminants are illustratedin Figure 3.FIGURE 3Proposed mechanism for high-sulphate-inducedpolioencephalomalacia (PEM)Sulfate Reductionin the RumenHigh sulphur or Sulphate(water and(or) feed) H 2S and S 2-Lung Tissue Damage?Secondary Viral orBacterial InfectionsSource: Adapted from Kung et al., 1998.H 2S InhalationCell DamagePEMS 2- AbsorptionPoor Animal Performance