The effect of Brachiaria decumbens (signal grass) on drug-metabolizing enzymes was studied in sheep. After 14 d of grazing a pure signal grass pasture, significant declines were observed in hepatic aminopyrine N-demethylase and aniline 4-hydroxylase (phase I biotransformation) and in conjugative enzymes UDP-glucuronyltransferase and glutathione S-transferase. Kidney enzymes were significantly decreased except for UDP-glucuronyltransferase. Enzyme activities were also compared for normal sheep and cattle livers and kidneys. Lower activities were found in cattle, indicating that factors other than biotransformation are responsible for the clincial tolerance of cattle to B. decumbens toxicity.
Spectroscopic examinations of purified extracts of the rumen content of sheep intoxicated by Brachiaria decumbens revealed the presence of a mixture of sapogenins, identified as 3-spirostanols. These isomeric steroid sapogenins (C27H44O3) are believed the toxic principles in causing toxicity in sheep after feeding on B. decumbens.
In addition to generalized icterus, enlargement of the liver and severe photosensitization, signal grass (Brachiaria decumbens) toxicity also caused ruminal stasis and a decreased rumen pH in sheep. Ruminal stasis, which occurred within 3 weeks of grazing on this grass, may be the effect of the toxin produced in the rumen rather than a sequele of a decreased rumen pH. Animals were anorexic and the volume of their rumen content was very much reduced.
Although Brachiaria decumbens was not toxic when fed to cattle, the infusion of rumen liquor from B. decumbens intoxicated sheep into the rumen of cattle produced evidence suggesting hepatic and renal dysfunction. Several biochemical changes were observed including increases in serum aspartate amino transferase, serum creatinine and blood urea nitrogen and a marked reduction in the plasma bromosulphthalein clearance.
Exposure to TEX-OE®, a patented extract of the prickly pear cactus (Opuntia ficus indica) containing chaperone-stimulating factor, was shown to protect common carp, Cyprinus carpio L., fingerlings against acute ammonia stress. Survival was enhanced twofold from 50% to 95% after exposure to 5.92 mg L(-1) NH(3) , a level determined in the ammonia challenge bioassay as the 1-h LD50 concentration for this species. Survival of TEX-OE®-pre-exposed fish was enhanced by 20% over non-exposed controls during lethal ammonia challenge (14.21 mg L(-1) NH(3) ). Increase in the levels of gill and muscle Hsp70 was evident in TEX-OE®-pre-exposed fish but not in the unexposed controls, indicating that application of TEX-OE® accelerated carp endogenous Hsp70 synthesis during ammonia perturbation. Protection against ammonia was correlated with Hsp70 accretion.
Severe neurological dysfunction was observed in sheep 4 weeks after grazing on Signal grass (Brachiaria decumbens). These neurological disorders included the stamping of forelegs, star-gazing, incoordination, head-pressing against the fence and circling movements. Histologically, numerous vacuolations of various sizes were observed in the white matter of the brain giving rise to a spongy appearance.
The effect of phenobarbitone against signal grass (Brachiaria decumbens) toxicity was studied in 26 male crossbred sheep. Grazing on signal grass significantly decreased the concentration of cytochrome P-450 and the activity of drug metabolizing enzymes, viz. aminopyrine-N-demethylase, aniline-4-hydroxylase, UDP- glucuronyltransferase and glutathione-S-transferase in liver and kidneys of affected sheep.Oral administration of phenobarbitone (30 mg/kg body weight) for five consecutive days before grazing on B. decumbens pasture, and thereafter, for three consecutive days every two weeks, resulted in significant increases in hepatic and renal activities of drug-metabolizing enzymes. The induction of drug metabolizing activity in sheep grazing on signal grass group was found to be lower than in animals given phenobarbitone alone. Induction by phenobarbitone provided a degree of protection against the toxic effects of B. decumbens as indicated by the delay in the appearance of signs of toxicity. Furthermore, these were much milder compared to those in the sheep not treated with phenobarbitone. The present study suggests that phenobarbitone-type cytochrome P-450 isoenzyme-induction may increase resistance against signal grass (B. decumbens) toxicity in sheep.
An attempt was made to clarify the association between zinc (Zn) and antioxidants due to Zn supplementation on lipid peroxidation occurring during Brachiaria decumbens intoxication. The concentration of Zn, copper, malondialdehyde (MDA), superoxide dismutase (SOD), and gluthathione peroxidase (GSH-Px) were determined in tissues. There was a gradual increment in the concentration of Zn and MDA in serum and hepatocytic SOD in groups given Zn + B decumbens. A decline in erythrocytic GSH-Px and SOD, and lower concentration of reduced glutathione in hepatocyte cytosols were also detected in these sheep. It is highly suggestive that Zn supplementation may depress antioxidant status and enhance lipid peroxidation during B decumbens intoxication.