Morphometric characteristic of the ultrastructure of rat lung mitochondria after administration of chrysotile asbestos to animals

he method of morphometric analysis was used to study ultrastructural changes in the mitochondria of the lungs of rats after a single intratracheal injection of chrysotile-asbestos dust into animals at doses of 25 mg and 50 mg. According to morphometric parameters, more serious changes were detected in mitochondria under the influence of asbestos at a dose of 50 mg, which were characterized by a significant increase in the area, perimeter and average diameter of the outer and inner membranes. The value of the area of the outer membrane of mitochondria in intact animals was 0.38±0.02 µm2, the perimeter was 2.52±0.11 µm, the average diameter was 0.75±0.03 µm, for experimental rats (asbestos 50 mg) the data the indicators turned out to be significantly increased and amounted to 0.59±0.04 µm2 (the area of the outer membrane), the perimeter was 3.67±0.19 µm, and the average diameter was 1.06±0.05 µm. For the inner membrane, these indicators in the control were as follows: the area of the inner membrane was 0.33±0.02 µm2, the perimeter was 2.40±0.12 µm, the average diameter was 0.71±0.032 µm, and for asbestos at a dose of 50 mg: 0.56±0.05 µm2 (internal membrane area), perimeter 3.68±0.21 µm, mean diameter 1.06±0.06 µm. Under the action of asbestos in lung cells, a significant decrease in the length of mitochondrial cristae was revealed: 9.11 ± 0.41 μm (control, intact animals), asbestos at a dose of 25 mg: 4.07 ± 0.33 μm and asbestos at a dose of 50 mg: 2.34±0.20 µm. Swelling and destruction of the cristae is observed, and this can be traced by morphometric parameters of the cristae diameter, which accordingly increased under the influence of 50 mg of asbestos by 90.9% (p<0.001). The obtained values of the area of the inner and outer membranes, the diameter and length of mitochondrial cristae made it possible to assess the degree of ultrastructural disorders of mitochondria, which may indicate mitochondrial dysfunction under the action of asbestos.