Sulphur availability and microbial fermentation in the fauna-free rumen

Abstract

The concentration of H2S and rate of feed digestion, VFA and methane production in the rumen were measured in sulphur deficient (-S) and S supplemented (+S) sheep while fauna-free (-P) and after refaunation (+P). The concentration of rumen H2S was increased by S supplementation but was not affected by the presence of protozoa. When fauna-free, -S sheep had reduced rates of feed digestion (30 v 48%/d), acetate synthesis (35 v 115 g/d) and methane synthesis (0.4 v 7.4 g C/d) compared to +S sheep and up to 36% (v/v) of total rumen gas was H2. When these sheep were given a single dose of 8.8 g Na2SO4, the proportion of methane increased and the proportion of H2 in rumen gas decreased. After refaunation of sheep, their rates of feed digestion, VFA production and methane production were higher and were not affected by the level of S. From this differential response to S deficiency by -P and +P sheep, it is concluded rumen protozoa increase the availability of S to other rumen microbes. This is probably because they degrade protein through to peptides and amino acids.

The effects of protozoa and of supplementation with nitrogen and sulfur on digestion and microbial metabolism in the rumen of sheep

“…The significant decrease in methane production when the basal diet was supplemented with S or N clearly indicates that supplementation has shifted fermentation to provide more products useable by the sheep and an increased growth efficiency of nonmethanogenic bacteria. This contrasts with the response of extremely S deficient sheep in which rumen H2 accumulates to abnormal levels and in which S supplements are known to stimulate methanogenesis and alleviate Hz build-up (Hegarty et al 1991). Fauna-free ruminants have previously been observed to produce less methane than faunated ruminants (Rowe et al 1985;Ushida et al 1986), but the difference was not significant in this study.…”

“…This may be an important adaptation t o aid survival of grazing ruminants on low-quality feeds, and is probably facilitated through the long retention time of protozoa in the rumen and the fact they are not reliant upon ammonia for growth. While rumen H2 S levels in Experiment 1 were adequate to maintain active fermentation, previous studies have shown that protozoa may also enable digestion to continue in sheep with less than 1 p H2S S/mL in the rumen (Hegarty et al 1991). This role of protozoa in maintaining rumen N and S supply has not previously been appreciated because most comparisons of faunated and fauna-free sheep have been made on S-and N-adequate diets which sustained rumen NH3 concentrations greater than 50 mgN/L (see Kreuzer 1986).…”

“…Cr was analysed with a Perkin-Elmer Model 360 atomic absorption spectrometer using an air and N 2 0 flame. The rates of feed digestion (in-sacco) and methane production in the rumen and the population density of rumen fungal sporangia developed on a leaf of wheaten hay incubated in-sacco in the rumen were estimated as previously described (Hegarty et al 1991). The concentration of H2S in rumen fluid was measured by the method of Bird (1972), except that p-hydroxymercuribenzoic acid was used as the titrant rather than mercuric acetate (Wronski 1960).…”

“…In recent studies in this laboratory the rate of digestion of marginally S deficient feed in the rumen was found to be slower in fauna-free than faunated sheep (Hegarty et al 1991). It is postulated this reduced microbial digestion in fauna-free sheep maintained on S deficient feed resulted from a reduced rumen availability of microbial protein precursors.…”

Methionine derivatives diminish sulphide damage to colonocytes--implications for ulcerative colitis.

“…[3][4][5] Most sulphide in the colon is produced by the anaerobic sulphate reducing bacteria, which require sulphate6 to facilitate removal of hydrogen produced by anaerobic bacteria in the colon,7-9 a process in which methane producing bacteria act competitively.10-2 The source of colonic sulphur is either ingested sulphate13 or sulphur extracted transmucosally from the circulation by the intestine.21 '7 The injurious potential of sulphur species in the colon was initially deduced from the ability of sulphated dextrans but not dextrans without sulphur to induce experimental colitis and colon cancer. 18 19 From a number of sulphur containing agents, sulphides proved most injurious to isolated human colonocytes20 by a mechanism proposed in part to be due to persulphide formation of activated SCFAs.21 Additional studies in humans showed that luminal sulphide concentrations in ulcerative colitis exceed that of control patients22 and that ulcerative colitis patients produce more sulphide from fermentative substrates compared with control patients.23 A role for sulphide in the causation of ulcerative colitis therefore seemed possible.…”