Biomedical subjects

J I Gray

Publications and source records attributed to J I Gray.

35 records · Page 2Linked to original sources

PubMed1988

Contribution of wood smoke to in vivo formation of N-nitrosothiazolidine-4-carboxylic acid: initial studies.

The effect of administering liquid smoke or smoked food products to rats on in vivo formation of N-nitrosamino acids was investigated. Rats treated by gavage with either cysteine, formaldehyde or nitrite excreted urine containing no detectable levels of N-nitrosothiazolidine-4-carboxylic acid (NTCA). All three precursor compounds were required for NTCA formation. Two liquid smokes, when administered to rats in combination with cysteine and nitrite also produced measurable quantities of NTCA. Ascorbate inhibited in vivo formation of NTCA by approximately 90% when given to rats simultaneously with cysteine, formaldehyde, and nitrite. alpha-Tocopherol was much less effective than ascorbate in blocking NTCA formation. When smoked bacon, smoked Swiss cheese, and chicken barbecued with a sauce containing smoke flavouring were fed to rats along with nitrate, NTCA was again detected in the urine.

Acetaldehyde↗

PubMed1986

Aflatoxin carryover and clearance from tissues of laying hens.

A feeding trial was conducted to determine the levels of aflatoxins deposited in the tissues of hens fed a diet contaminated with 3310 micrograms AFB1/kg and 1680 micrograms AFB2/kg for 4 wk. At the end of aflatoxin feeding, the livers were pale, enlarged and haemorrhagic and the ovaries were significantly smaller than those from control hens and contained only small ova. Only a small fraction of the aflatoxins consumed was deposited in the tissues, either as the original compounds or as their metabolites, which were widely distributed in all tissues. The highest levels of aflatoxins were detected in the gizzard, kidneys and liver, with average total concentrations of less than 3 micrograms/kg. The lowest residue levels were detected in the breast, blood serum and leg, with breast muscle having a total concentration of less than 0.1 microgram/kg. Two days after removal of the contaminated feed, aflatoxin residues in all tissues had decreased markedly, with no aflatoxins being detected in the heart or spleen. No aflatoxin residues were detected in the breast, leg, gizzard and ovaries of hens killed 8 days after withdrawal, or in the kidneys and blood at 16 days. However, one of seven hens had measurable amounts of AFB2 in the liver 32 days after withdrawal. Although few residues were detected in most tissues after 8 days on the aflatoxin-free diet, variation existed between tissues and between individual hens in the amount of time required to achieve tissue clearance.

Aflatoxins↗

PubMed1985

Aflatoxin deposition and clearance in the eggs of laying hens.

Hens fed a diet containing 3310 micrograms of AFB1 and 1680 micrograms of AFB2 per kg feed for 28 days showed a significant decrease in egg production and egg weights by wk 3 and 4 of feeding, respectively. Transfer of aflatoxins to the eggs occurred rapidly, reaching maximum levels after 4-5 days, and remained relatively constant throughout aflatoxin feeding. The mean values for combined residue levels in eggs were less than 0.5 microgram/kg. Levels of AFB2, AFM1 and AFM2 were similar in yolk and albumen while levels of B1 and B2a were higher in the yolk. Upon removal of the aflatoxin-containing diet, residues in eggs decreased rapidly. Clearance of aflatoxin residues from the albumen occurred faster than from the yolk. Thus, no residues were detected in the albumen and in the yolk after 5 and 7 days of withdrawal, respectively. No aflatoxin residues could be recovered from whole eggs after feeding the aflatoxin-free diet for 4 days.

Aflatoxins↗

PubMed1985

Broiler aflatoxicosis with recovery after replacement of the contaminated diet.

Broiler chickens were fed a diet containing 2057 and 1323 micrograms/kg feed of aflatoxins B1 and B2, respectively, for 35 d. Effects of aflatoxins on growth, food consumption, efficiency of food utilisation and manifestations of aflatoxicosis were compared with control birds at the end of the feeding trial and at 1, 2, 4, 8 and 16 d after replacing the contaminated feed. No difference in food consumption was observed between the controls and the aflatoxin-fed chickens, but efficiency of food utilisation was decreased from 2.2 for the controls to 2.4 g food/g gain for the group fed aflatoxins. Aflatoxins caused depressed growth and enlargement of the kidney, liver, heart and gall bladder. Haemorrhagic spots were present on the surface of the muscles and some of the livers. Most livers from aflatoxin-fed birds were pale and infiltrated with lipid. After withdrawal of the food containing aflatoxins, all apparent gross lesions of aflatoxicosis disappeared, with no evidence of any lesions 8 d after removal of the contaminated diet.

Aflatoxin B1↗

PubMed1984

Tissue deposition and clearance of aflatoxins from broiler chickens fed a contaminated diet.

A study was conducted to determine aflatoxin levels in the tissues of broiler chickens that had been fed a diet containing 2057 micrograms aflatoxin B1 and 1323 micrograms aflatoxin B2/kg for 35 days. Results showed that aflatoxins were deposited in all tissues. The highest levels of aflatoxins were present in the gizzards, livers and kidneys. There was evidence that the high levels of aflatoxins B1 and B2 in the gizzards might have been caused by contamination by the gizzard contents during the slaughtering process. After feeding the aflatoxin-contaminated diet for 35 days, mean values for the combined aflatoxins were less than 3 micrograms/kg of tissue. Four days after withdrawal of the aflatoxin-contaminated ration, there were no detectable amounts of aflatoxins in any of the tissues. The results indicate that broiler chickens rapidly clear aflatoxins from their tissues once they are transferred to an aflatoxin-free diet.

Aflatoxins↗

PubMed1984

Further factors influencing N-nitrosamine formation in bacon.

The possible relationship of unsaturated fatty acids in adipose tissue to the formation of N-nitrosamines in bacon was evaluated by trials in which pigs were fed regular (control), tallow-, coconut fat- and corn oil-supplemented diets. Bacon prepared from pigs fed corn oil-supplemented diets contained significantly higher levels of N-nitrosopyrrolidine and N-nitrosodimethylamine than did control bacon samples; however, bacon produced from pigs fed a coconut fat-supplemented diet contained significantly lower levels of N-nitrosopyrrolidine. Fatty acid analyses of the adipose tissue of the bacon samples indicated that N-nitrosopyrrolidine levels in bacon correlated well with the degree of unsaturation of the adipose tissue. N-nitrosothiazolidine was detected in both brine-cured and dry-cured bacon at levels generally below 4 micrograms/kg. However, its formation was greatly reduced by the inclusion of alpha-tocopherol in the cure. The role of woodsmoke in N-nitrosothiazolidine formation in bacon is discussed.

Adipose Tissue↗

PubMed1981

Some toxic compounds produced in food by cooking and processing.

Both cooking and processing of food can produce toxic compounds in food, if the appropriate precursors are present. N-Nitrosamines, polycyclic aromatic hydrocarbons and phenolic compounds, lipid polymerisation products resulting from deep-fat frying, lipid oxidation products, Maillard-browning products and other products of protein reactions are discussed as well as their formation, concentration and control. The conclusion points out that contamination of human food is almost impossible to avoid and must be considered together with the beneficial effects of food processing on food safety, flavour, shelf-life and convenience.

Chemical Phenomena↗

PubMed1978