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In mammals, the damage to the hair cells of the inner ear due to exposure to noise or other ototoxic agents is irreversible. In fish, reptiles and birds, however, the hair cells may regenerate, probably from the supporting cells. This regeneration process in the inner ear is being intensively examined in animals in the hope of curing the sensorineural hearing loss in human subjects in future. The aim of the study was to assess hair cell regeneration in the inner ear of chicks after exposure to industrial noise, depending on the level of exposure. The birds were exposed either to the noise at the level of 110 dB (A), 4 hours a day, for 5 consecutive days, or at the level of 125 dB (A), 8 hours a day, for 5 consecutive days. The results confirm that the regeneration starts immediately during the period of recovery from acoustic trauma, and the supporting cells are the main source for new, developing hair cells. Moreover, we found that the complete damage to hair cells is not necessary to the proliferation of supporting cells and that the intensity of proliferation of these cells depends on the level and time of exposure.

The basilar papilla corresponds to the cochlea of mammals and is becoming a common model of assessment of the regeneration process which takes place after the damage to the inner ear caused by noise or ototoxic drugs. In this study the morphology of a chick's basilar papilla in light and electron microscopy is described. There are two types of hair cells (sensory cells): the tall hair cells and the short hair cells, whose morphology and pattern of innervation are different. The tall hair cells correspond to the inner hair cells in mammals, which are responsible for sound transduction. They are mainly innervated by the afferent (cochlear) fibers. The short hair cells correspond to the outer hair cells in mammals, which are responsible for the sound amplification. They are mainly innervated by the efferent fibers. The supporting cells, whose morphology is also described in the study, separate the hair cells from each other and from the basilar membrane. They are considered to be a source for regenerating hair cells.

The effects of combined inhalatory exposure to m-xylene and toluene on the rat hepatocytes were investigated. Limited proliferation of smooth endoplasmic reticulum and increase of the number of lysosomes were observed in hepatocytes after 3-months of single exposure to 1000 ppm of m-xylene and toluene. Moreover, mitochondria increased in most of hepatocytes. After combined exposure to mixture of m-xylene and toluene at concentrations of 500 + 500 ppm, respectively, the types of ultrastructural changes in hepatocytes followed the pattern observed after exposure of each of the single organic solvent. However, proliferation of the smooth endoplasmic reticulum was more eminent. The hepatocytes ultrastructure of rats exposed to 100 ppm of m-xylene and toluene for 6 months were similar to that observed in rats exposed to 1000 ppm of m-xylene for 3 months. In rats exposed to a mixture of m-xylene and toluene for 6 months, the ultrastructural changes in hepatocytes were a combination of those observed after a single exposure to each of the organic solvent. It may be concluded that changes in the hepatocytes ultrastructure were an adaptive rather than a toxic effect. Because in the case of combined exposures the doses were half of those used in single exposures, the additive effect on the proliferation of smooth endoplasmic reticulum was observed in the rat liver after combined exposure to toluene and m-xylene using electron microscopy.

Studies on rats treated for 8 months with ethanol (10% solution in drinking water) and simultaneously exposed to xylene vapour (12,000 mg/m3, 5 hr daily) for the last 9 days revealed that the chemicals exert additive stimulatory effect on hepatic microsomal monooxygenase: the activity of aniline p-hydroxylase increased by 380%, microsomal ethanol oxidizing system by 92%, NADPH-cyt. c reductase by 30% and the level of cytochrome P-450 by 70%. The changes were accompanied by a marked proliferation of smooth endoplasmic reticulum (a subcellular site of cytochrome P-450 monooxygenases in the hepatocytes) and an increased NADPH-Fe2+- and ascorbate-Fe2+-driven lipid peroxidation in microsomal membranes--a potential toxic mechanism. Interaction of ethanol and xylene with cytochrome P-450 monooxygenases may enhance metabolic capacity of the liver and in consequence modify biological/toxic effects of occupational exposure to solvents in the case of alcohol abuse.

Female Wistar rats were injected (sc) every second day for 8 weeks with Cd (0.25 mg/kg) as CdCl2. After only a 2-week exposure, when cadmium (Cd) concentration in liver was about 13 micrograms/g, ultrastructural examinations revealed some irregular ergastoplasm systems and significant proliferation of smooth endoplasmic reticulum in the hepatocyte ultrastructure. The increase in Zn content occurred simultaneously with the increase in Cd concentration in the liver (Zn to Cd ratio was 1:1). In the kidneys after a 3-week exposure, when Cd concentration was 7 micrograms/g, the concentration of endogenous Cu increased. At the same time the urinary excretion of that metal was considerably higher than that of the control group. In the kidneys after a 4-week exposure, when Cd concentration in this organ exceeded 10 micrograms/g tissue, injured brush border microvilli and swollen mitochondria in the proximal convoluted tubular cells were seen. In renal corpuscules, fusion between the podocyte pedicles was also found. The changes in renal cortex ultrastructure became more pronounced when Cd concentration in kidney was increasing. Necrotic changes in the examined organ were observed when Cd concentration increased to about 30 micrograms/g tissue. The critical concentration in renal cortex of about 200 micrograms/g tissue should be revised. The present margin of safety with regard to risk of renal effects is small.