In vitro action of quartz on alveolar macrophage lipid peroxides.

The in vitro effects of quartz particles on the lipid peroxide rate were measured on guinea pig pulmonary alveolar macrophages (PAMs). As controls, either PAMs alone or exposed to inert dust were used. The amount of lipid peroxide resulting after one-hour incubation was determined by means of the thiobarbituric acid test (TBA). The results showed that quartz induced a substantial increase of lipid peroxide in PAMs compared with both samples (dust-free or exposed to corundum). The influence of pretreatment of quartz by polyvinylpyridine-N-oxide (PVPNO) and by mineral water containing carbonate and chloride ions was also studied.

Effect of asbestos on lipid peroxidation in the red cells.

In vitro exposure of red cells to vie International Union against Cancer (UICC) standard reference asbestos samples resulted in an increase of thiobarbituric acid substances. Chrysotiles developed the largest amounts of lipid peroxides, followed by anthophyllite, amosite, and crocidolite in decreasing order. Compared with the control samples erythrocytes free of dusts, all types of the asbestos examined disclosed significant differences. The results obtained provide support for the cytotoxic potential of amosite and crocidolite and, on the other hand, suggest that a lipid peroxidation of unsaturated fatty acids may be involved in the mechanisms(s) of membrane-damaging effects of asbestos dusts.

Effect of cadmium chloride on adrenal function in the white rat.

Wistar female rats were given 0.5 mgCd+2/kg b.w. in the form of CdCl2, in drinking water, administered by intragastric probe daily for 90 days, and a dose of 5 mg/Cd+2/kg b.w. subcutaneously administered once a week, for a period of 30 days. The adrenal gland functional status was investigated by glycogen, total lipid, ascorbic acid content, organ weight and histometric measurements. No changes were observed in the animal which received intragastric Cd. Subcutaneous administration of 5 mgCd+2 determined a significant increase in organ weight as against the controls, with a widening of the fascicular stratum, and a marked decrease in glycogen, total lipids and ascorbic acid, parallel with high values of 17-ketosteroids. The data revealed a toxic effect of cadmium upon the adrenals, evidenced by a hyperactivity. Adrenal glycogen, total lipids and ascorbic acid depletion evoked a stimulated ACTH hormone release with a high rate of excreted 17-ketosteroids.

Short-term systems to assess thiophosphoryl chloride standards.

The rat acute oral LD50 value of PSCl3 is 750 mg per kg body weight. A rat 90-day oral feeding study at dose levels of 7.5 mg (P1) and 37.5 mg (P5) per kg resulted in increased body weight gain. Other responses inconsistently varied between dose levels. At 7.5 mg kg-1, a trend towards enhancement of relative weight of liver, spleen, kidney and adrenals was noted; at 37.5 mg kg-1, decreasing relative spleen and adrenal weights were observed. The most of the hematological and biochemical changes in blood serum cannot be believed to be transitory adaptive changes, but valid toxic effects. On the other hand, there are some indicators that suggest a possible trophic effect of this compound. However, the reversible dystrophic changes in liver, as well as the histochemical and histoenzymical results, require us to take into account that inactive chronic hepatitis could be reactivated by further toxic insult. A teratology study demonstrated increased number, body weight and length of fetuses, without apparent pathological events (tumors, external malformations). A mutagenicity test performed on rat femoral bone marrow after 30-days feeding of 37.5 mg kg-1 did not indicate any significant change in the incidence of chromosomal aberrations, compared with the control group. The recommended maximum allowable concentration in the working zone for thiophosphoryl chloride in air was set at 3 mg m-3.