In this experimental study, the effect of cadmium on cold and restraint stress-induced gastric lesions has been studied. Rats received 15 micrograms/mL cadmium-containing water for 30 d, and at the end of this period, they were subjected to cold and restraint stress. Cadmium accumulation in gastric mucosa was associated with increased mucosal lesions, as well as decreased mucin and PGE2 levels in rats exposed to cadmium. Stress-induced mucosal injury was more pronounced, and the hemoglobin leakage into gastric lumen owing to breakdown in the barrier was 17.30 +/- 3.45 micrograms/mL in control and 35.71 +/- 6.18 micrograms/mL in treated rats. Our data suggest that high cadmium intake facilitates the occurrence of stress-induced mucosal lesions by diminishing the mucin content and PGE2 generation in gastric mucosa.

An important explanatory theory for the mechanism of postexercise proteinuria is that angiotensin II could be inhibited by angiotensin converting enzyme inhibitors. Because of the kininase effect of the angiotensin converting enzyme, it is unclear whether the kallikrein-kinin system contributes to the effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. The aim of this study was to evaluate any possible involvement of the kallikrein-kinin system in the therapeutic effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. We evaluated urinary protein levels in exhausted rats receiving an angiotensin converting enzyme inhibitor (enalapril) or an angiotensin II type I receptor antagonist (losartan). Enalapril (30 mg/kg/day, two days) or losartan (20 mg/kg/day, two days) were given to animals using an intragastric catheter. Urinary protein levels increased (41 %) in rats which were exhausted via treadmill running (p < 0.05). In animals that received drug treatment (enalapril or losartan), but did not exercise to exhaustion, urinary protein levels were not different from the control group. Urinary protein levels were found to be significantly lower (p < 0.05) in animals which performed acute exhaustive exercise after enalapril or losartan administration, compared to rats which were exhausted without drug administration. Inhibition of postexercise proteinuria by either enalapril or losartan suggested that angiotensin II plays an important role in postexercise proteinuria, however, it appears the kallikrein-kinin system is not involved in angiotensin converting enzyme inhibitors effect.

Since the kidney is the main target organ for many metals including cadmium, the generation of the products of lipid peroxidation due to accumulation of these toxic metals in the kidney may have importance in the mechanism of their nephrotoxicity. In order to test this hypothesis, we carried out an experimental study in rats. The functions and the levels of tiobarbituric acid reactive substances (TBARS) of the kidney were investigated in animals receiving 15 micrograms/ml aqueous Cd solution for 30 days. Due to cadmium accumulation in kidney cortex, the ratio of Cd/Zn increased significantly and this increase was associated with elevated TBARS in both renal cortex and medulla. The content of TBARS in renal cortex rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p<0.01) and GFR decreased to 390.5 +/- 109.4 from 1008.7 +/- 4.8 microliters/min (p<0.01) in cadmium exposed animals. Daily coadministration of selenium, vitamins A, C, E did not reverse the adverse effect of cadmium on kidney function, despite the significant decrease in cortex TBARS levels (p<0.01). In conclusion, these data suggest to us that lipid peroxidation assessed by TBA test may not be the only mechanism in cadmium induced nephrotoxicity.

Pregnant Swiss albino rats were divided into control (C) and cadmium (Cd) groups. Control animals received tap water while the Cd group received Cd as CdCl 2 in their drinking water. The rat pups were separated from their mothers 22 days after birth. 78 young rats were divided into two main groups: controls (Ci, C 2 , C 4 ) and cadmium groups (Cd], Cd 2 , Cd,»). Each sub-group included 13 rats. On postnatal days 30, 60, and 120, spectral analysis of EEGs recorded from the parietal lobes of all groups of rats was computed by fast Fourier transform (FFT) algorithm. The amplitude maxima were found to occupy the frequency bands of 1-2, 2-4, 4-6, 6-8, 8-16, and 16-30 Hz. The decibel (dB) values of the maxima were significantly decreased in Cdi and Cd 2 groups compared with the corresponding control groups in all the frequency bands except 16-30 Hz. A significant amplitude (dB) decrease was observed in all the frequency bands of the Cd 4 group compared with the C 4 group.

Pregnant Swiss albino rats were divided into three groups: control (C), cadmium (Cd) and non-cadmium (NCd) groups. Control animals received tap water; the Cd rats received Cd as CdCl2 in their drinking water during the experimental period, while the NCd group was given Cd during pregnancy, and given tap water after birth. Twenty-two days after birth, 15 rats (for each group) were taken from their mothers and continued to be treated with Cd (Cd group) or tap water (C and NCd groups) for an additional 38 days. After the treatment period, somatosensory evoked potentials (SEPs) of the three groups were recorded from central (Cz) referenced to frontal (Fz) following left posterior tibial nerve (PTN) stimulation. Amplitude spectra of SEPs were computed by fast Fourier transform (FFT) algorithm. There was a significant amplitude decrease in 1-3.5 Hz in the NCd group and 1-3.5 and 14-20 Hz frequency bands of the Cd group compared with the control group.