Effect of dietary formates on growth performance, carcass traits, sensory quality, intestinal microflora, and stomach alterations in growing-finishing pigs.

Three experiments were conducted to evaluate the effect of adding salts of formic acid to diets for growing-finishing pigs. In Exp. 1, 72 pigs (23.1 kg and 104.5 kg initial and final BW) were used to evaluate the effect of Ca/Na-formate and K-diformate on performance and carcass traits. Treatments were organized in a 2 x 3 factorial arrangement with two feeding regimens (limit and semi-ad libitum feeding) and three diets (control, .85% Ca/Na-formate, and .8% K-diformate). No significant feeding regime x diet interaction was found. The K-diformate diet increased overall ADG of pigs compared with the control and Ca/Na-formate diets, but had no effect on ADFI or gain/feed (G/F) ratio. Neither K-diformate nor Ca/Na-formate had any effect on carcass lean or fat content. In Exp. 2, 10 limit-fed pigs (24.3 kg and 85.1 kg initial and final BW) were used to study the effect of K-diformate on performance and sensory quality of pork. Adding .8% K-diformate to diets increased ADG (P < .13) and G/F (P < .04), but had no effect on sensory quality of the pork or content of formate in liver, kidney, or muscle tissue of pigs. In Exp. 3, 96 limit-fed pigs (27.1 kg and 105 kg initial and final BW) were used to determine the effect of adding K-diformate to diets on performance, carcass traits, and stomach keratinization and(or) lesions. Adding K-diformate (0, .6, or 1.2%) to diets increased ADG and ADFI (linear P < .01). The K-diformate reduced the percentage of carcass fat (linear P < .03) and fat area in the cutlet (linear P < .09) and increased percentage lean in the ham (linear P < .01), flank (linear P < .02), loin (linear P < .09), and neck and shoulder (linear P < .09). The K-diformate had no negative effect on stomach alterations. In Exp. 3, the concentration of coliform bacteria in the gastrointestinal tract was evaluated in eight control and eight 1.2% K-diformate-fed pigs. The K-diformate reduced the number of coliforms in the duodenum (P < .03), jejunum (P < .02), and rectum (P < .10) of pigs. In conclusion, K-diformate improved growth performance and carcass quality of growing-finishing pigs, whereas Ca/Na-formate had no effect. K-diformate had no adverse effect on sensory quality of pork or on stomach alteration scores.

Effect of dietary arginine on urinary nitrate excretion in germ-free rats.

The effect of dietary arginine on the endogenous synthesis of nitrate in germ-free rats was investigated. The animals were fed, for up to 18 days, purified diets containing either casein or lactalbumin (proteins differing in arginine content) with or without additional free arginine. Urine was collected from all animals for 4 days, and the animals were then dosed ip with Escherichia coli lipopolysaccharide (LPS) to stimulate nitrate synthesis and urine collected for a further 4 days. The urine samples were analysed for nitrate by ion chromatography. Although the excretion of nitrate was markedly stimulated by LPS treatment, there were no significant effects of protein source or arginine supplementation of the diet.

Cells, bilirubin and light: formation of bilirubin photoproducts and cellular damage at defined wavelengths.

Cultured cells from one human and one murine cell line were treated with bilirubin and irradiated with visible light of different wavelengths, either from phototherapy lamps or from a Xenon/Mercury lamp equipped with a monochromator. Bilirubin bound to human serum albumin was also irradiated with light. After irradiation, the bilirubin and its photoisomers were extracted and analysed with High Pressure Liquid Chromatography. The formation of single strand breaks in the DNA of treated cells was studied using a fluorescence marker. Cytotoxicity in the mouse skin cell line was measured by loss of the ability to form visible colonies in vitro. Green light exposure favours the production of lumirubin, while blue light causes more DNA damage and cytotoxicity. Green light may be more efficient and safer than shorter wavelength exposure when treating jaundiced newborns with phototherapy.

Endogenous N-nitrosation in man assessed by measurement of apparent total N-nitroso compounds in faeces.

The faecal concentration of substances responding to the chemical test for N-nitroso compounds (apparent total N-nitroso compounds, ATNC) was investigated in human subjects consuming their normal free-choice diet. Concentrations ranged from 40 to 590 micrograms (N-NO)/kg faeces. To ascertain the likely relative contributions of endogenous ATNC formation and preformed, dietary ATNC, the subjects consumed a diet low in nitrate and ATNC for 8 days. At the end of this period, ATNC had decreased substantially with concentrations ranging from below the 40 micrograms (N-NO)/kg detection limit up to 143 micrograms (N-NO)/kg, mean 82 micrograms (N-NO)/kg. On supplementing this diet with 300 mg nitrate/day, faecal ATNC levels increased markedly. On the third day of this regime, values were in the range 73-714 micrograms (N-NO)/kg with a mean of 307 micrograms (N-NO)/kg. The results, together with the known limited occurrence of ATNC in the majority of foodstuffs so far tested, generally non-detectable or less than 100 micrograms (N-NO)/kg, suggest that endogenous formation via species derived from dietary nitrate is likely to be an important source of ATNC in human faeces.

Nitrate and nitrite concentrations in human saliva: variations with salivary flow-rate.

Salivary nitrate concentration has often been used as a measure of human intake of nitrate. However, our findings indicate that this is not a reliable indicator because the nitrate concentration varies with salivary flow-rate and thus depends on the sampling procedure. Parotid or whole saliva was collected from up to six volunteers under carefully controlled conditions. The effects of stimulating saliva production by chewing on silicon tube (mechanical stimulation) or by sucking citric acid from cotton wool (gustatory stimulation) were investigated. Chewing decreased the average nitrate (plus nitrite) concentration in whole saliva by 59% and the nitrate concentration in parotid saliva (which does not contain nitrite) by 53%, relative to unstimulated saliva. Citric acid stimulation decreased the average parotid salivary nitrate concentration by 88%. Stimulation of salivary secretion increased the total salivary nitrate output and the extent of reduction of nitrate to nitrite for most subjects. The unstimulated parotid salivary nitrate concentration was, on average, 2.8 times the nitrate plus nitrite concentration in unstimulated whole saliva.