Influence of ingested lead on the distribution of lead, iron, zinc, copper and manganese in bovine tissues.

Five groups of cattle were dosed daily with either 0, 6.3, 7.8, 9.8 and 12.2 mg of lead/kg of body weight for 118 days or for as long as they lived, and tissue concentrations of lead, iron, zinc, copper and manganese were determined post-mortem. Mean intakes of lead for the five groups were 0, 34, 165, 55 and 57 g respectively. Lead accumulated in all tissues of treated animals and was greatest in kidneys and liver. The accumulation of lead and iron in livers of the treated animals appeared to be related to lead intake. The zinc and iron concentrations in liver were significantly increased by the ingestion of lead whereas the copper concentrations in liver and heart and the manganese concentration in kidney were significantly decreased by the ingestion of the lead.

Chronic lead poisoning in horses.

Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days 106 to 295). This period was designated phase 2. The smallest daily dose in phase 2 was set at about 125% of the largest daily dose in phase 1. The doses in each group was increased by about 125% of that of the previous group, as was done in phase 1. Seven horses died or were euthanatized after 18 to 190 days of phase 2 (123 to 295 days after the 1st dose). One horse in group I did not develop any clinical signs of intoxication. Dose-related responses were unnoticed with doses larger than 15.3 mg/kg/day. All horses given lead had increased blood lead and serum iron concentrations. During phase 2, the hematocrit (erythrocyte volume) and hemoglobin contents were depressed. The lead concentration in kidney, liver, spleen, pancreas, brain, bone, and heart was increased in the treated horses. The dose level required to produce lead intoxication was greater than that reported for cattle and that estimated in epizootiologic studies of horses.

Photosensitization in cattle and sheep caused by feeding Ammi majus (greater Ammi; Bishop's-Weed).

Feeding Ammi majus to cattle and sheep caused photosensitization in both species. It also caused photosensitization in human beings who had dermal contact with the plant and subsequent exposure to sunlight.

Effects of daily oral subtoxic doses of a wet lead-based paint on cattle.

Cattle were dosed daily with a wet lead-based paint at a rate of about 6 mg of lead per kg per day for 60 weeks. The cattle did not exhibit overt symptoms of lead toxicosis. Blood and fecal samples collected during the study, and tissue samples obtained at slaughter of the animals were analyzed for lead by atomic absorption spectrophotometer equipped with a graphite furnace. Levels of lead in whole blood generally did not exceed 0.5 ppm. The residues of lead in feces reached as high as 1000 ppm. Highest residues in tissues were in calcified bone, the kidney cortex, kidney medulla, and then in liver. Residues of lead in muscle, brain, spleen, and bone marrow were similar to residues of lead in the control animal. Calves born to 2 test animals had elevated levels of lead in bone, kidney and liver.

A unique intracellular aberration related to hexachlorobenzene ingestion.

Liver of rats fed hexachlorobenzene (HCB) at concentrations of 1, 5, 10 and 25 ppm for 3 to 12 months was studied by electron microscopy. A unique hepatic cellular change that seemed related to HCB ingestion occurred in more than half of the rats given 5 ppm or more HCB. The changes appeared as degeneration of lipid vesicles into a form of autophagic vacuole or storage vesicle. Degeneration of the lipid vesicles appeared to be by autodigestion, i.e., by endoplasmic reticulum encapsulation and partial digestion in the manner typical of other autophagic vacuoles. It is postulated that autodigestion may represent a way for the cell to eliminate fat-stored HCB.

Mirex-induced hepatic changes in chickens, Japanese quail, and rats.

Mirex was fed in the diet to chickens at 0 to 160 ppm for 12 and 16 weeks, to Japanese quail at 0 to 80 ppm for 12 weeks, and to rats at 0 to 100 ppm for 2 and 4 weeks. Mirex did not affect the concentration of protein or cytochrome P450 in hepatic microsomes of chickens or Japanese quail, nor did it affect hydroxylation of aniline or demethylation of aminopyrine. However, structural changes were apparent in livers of chickens fed mirex at 10 ppm and above and included regions of necrosis and nonspecific cellular aberrations and alterations of sinusoids and bile canaliculi. Mirex caused liver enlargement in rats and increased microsomal protein and cytochrome P450 but did not affect hydroxylation of aniline or demethylation of aminopyrine. Hepatic structural changes in rats that were associated with mirex included proliferation of smooth endoplasmic reticulum and degeneration of some bile canaliculi.

Ultrastructural changes in liver of the rat fed hexachlorobenzene.

Changes in hepatic ultrastructure were observed in rats given hexachlorobenzene (HCB) as a component of the diet in concentrations of 5, 10, and 25 ppm for 3, 6, and 12 months. A significant change was in the cellular regions normally containing smooth endoplasmic reticulum (SER). Sometimes the SER proliferated and at other times it appeared to be replaced by quantities of storage product presumed to be glycogen. Proliferation of SER was often associated with the smaller doses of HCB and the increase in storage products with the larger doses of HCB. However, dose relationships were variable. The most significant changes were in mitochondria which became elongated or swollen. Swollen mitochondria were occasionally as large as nuclei. Usually only a fraction of the mitochondria in a cell appeared abnormal. Storage bodies 1 to 4 mum in diameter developed in some cells. These bodies were surrounded by a double membrane derived from the endoplasmic reticulum and may have been the partly digested remains of degenerated mitochondria.

Partial lobectomy of bovine liver: a new biopsy technique.

A surgical technique has been developed for partial lobectomy of the bovine liver to obtain greater than 25 gram liver samples. Vertical mattress sutures, backed with plastic tubing, were replaced in the liver near the incision line to provide hemostasis. Hemostasis of the cut surface of the liver was adequate in each case. Postoperative recovery was uneventful and only minor adhesions were found later by laparotomy and at necropsy.