Cd In Testis Research Articles

Egg white hydrolysate prevents reproductive impairments induced by cadmium in rats

Abstract Here, we investigated the ability of an egg white hydrolysate (EWH) to counteract the reproductive toxic effects induced by Cd in rats. 3-month-old male Wistar rats were treated for 14 days: (a) Untreated group (distilled water i.p.); (b) Cd group (CdCl2 at 1 mg/kg body weight i.p.); (c) EWH group (1 g/kg body weight/day per gavage); (d) CdEWH group (CdCl2 with EWH). Cd exposure was able to be accumulated in testis and epididymis, increasing oxidative stress and compromising sperm quality and daily sperm production. Co-treatment with EWH prevented increased deposition of Cd in testis (Untreated: 0.04 ± 0.02; Cd: 4.68 ± 1.03*; EWH: 0.01 ± 0.00; CdEWH: 1.85 ± 0.25# μg Cd/g dry tissue p

Effect of ascorbic acid supplementation on testicular steroidogenesis and germ cell death in cadmium-treated male rats

Cadmium (Cd) is one of the environmental pollutants affecting various tissues and organs including testis. Harmful effect of Cd in testis is known to be germ cell degeneration and impairment of testicular steroidogenesis. Animals treated with high doses of Cd (0.2 and 0.3 mg/100 g BW) showed a significant decrease in serum testosterone (T) level, but a significant induction of testicular lipid peroxidation levels. TUNEL assay showed that low doses of Cd (0.13 and 0.15 mg/100 g BW) exhibited typical characteristics of apoptosis while high doses of Cd caused more necrosis than apoptosis. In contrast, supplementation with ascorbic acid reduced testicular lipid peroxidation levels. Ascorbic acid supplementation restored testicular 3β-hydroxysteroiddehydrogenase (HSD) and 17β-HSD enzyme activities, 3β-HSD and cytochrome P450 side chain cleavage (P450 scc) mRNA levels and serum T concentration to normal in Cd-administered rats. Moreover, administration of ascorbic acid prevented germ cell apoptosis as demonstrated by the reduced number of TUNEL-positive cells in germinal epithelium and inhibited Cd-induced necrosis. These results indicate that ascorbic acid have protective roles in vivo on the Cd-induced overall testicular damage including impaired steroidogenesis and germ cell death possibly through scavenging the reactive oxygen species generated by Cd administration.

Cadmium-induced testicular damage in a rat model of subchronic intoxication.

Background: Cadmium (Cd)-induced testicular damage in relation to spermatogenesis has not been well studied. We studied the mechanism of Cd-induced testicular damage in a rat model of subchronic intoxication. Methods: Male Sprague-Dawley rats were subcutaneously injected with 0.6mg Cd/kg per day for 6weeks. The concentration of Cd in urine, serum and testes was measured by using atomic absorption spectrophotometry. Testicular damage was evaluated by counting the spermatogonia (SG) and spermatocytes (SC) on one cut-surface of five seminiferous tubules in stages VII or VIII of spermatogenesis every week. The location of intratesticular cadmium was determined by using oxine-fluorescent cytochemistry. Results: There were no differences in the testes/bodyweight ratio between the study and control groups. The concentration of Cd in the testes increased more than 100-fold that in serum after week2, suggesting active testicular Cd accumulation (1-3mg/g tissue). Cadmium accumulation was detected in SG and SC. The number of SG and SC diminished significantly in the study group (week2: SG 74%, SC 90%; week4: SG 47%, SC 75%; week6: SG 30%, SC 54% of the control, respectively). Conclusions: Cadmium accumulated in SG and SC, consequently reduced the number of these cells, and disturbed the spermatogenesis in this rat model of subchronic Cd intoxication. Therefore, the number of SG decreased in this rat model of subchronic Cd intoxication. (Reprod Med Biol 2002; 1: 59-63).

Concurrent exposure to lead, manganese, and cadmium and their distribution to various brain regions, liver, kidney, and testis of growing rats.

Growing rats were exposed to 5 mg/L Pb,ad libitum in drinking water, and administered low or high doses of Mn and Cd intraperitoneal (i.p.) for 30 days. Some groups of animals were also administered combinations of Pb + Mn and Pb + Cd in an identical manner. Analysis of Pb, Mn, and Cd in tissue samples showed the expected dose-dependent accumulation when the metal was administered singly. However, combined treatment produced different types of metal shift in different tissues. Enhanced accumulation of all three metals in the brain, Mn in liver, Pb in kidney and Cd in testis and kidney after combined exposure may make target organs vulnerable to the toxic effects of metals, even when encountered at low concentrations. Further, the decreased levels of blood Pb after combined treatment with Cd or Mn suggests that the significance of blood Pb level as a diagnostic aid for Pb toxicity in coexposed conditions may not be of much value. Changes in the metallic distribution within the tissues after coexposure may be the result of a competition between the administered metals for common binding sites.

Resistance to cadmium-induced necrosis in testes of inbred mice: Possible role of a metallothionein-like cadmium-binding protein

Altered accumulation and subcellular disposition of testicular Cd were examined as possible explanations for the resistance to Cd-induced testicular damage observed in certain inbred strains of mice. Mouse strains susceptible ( 129 J ) or resistant A/J to Cd-induced testicular necrosis were injected iv with 10 or 45 μmol CdCl 2/kg, respectively. This dosing regimen compensated for decreased Cd accumulation by A/J testes and established similar concentrations of Cd in testes of both strains (approximately 4 nmol Cd/g tissue). Twenty-four hours later, 129 J testes showed marked interstitial hemorrhage and seminiferous tubule necrosis, while A/J testes showed no microscopic evidence of damage. Two hours postinjection, no histopathologic changes were detected in testes of either strain; however, A/J testes had 15% more Cd associated with the cystosol than 129 J testes, and three times more Cd bound to a 14,500 MW cytosolic protein which had gel filtration and ion-exchange chromatography properties in common with metallothionein (MT). Therefore, resistance of A/J testes to Cd does not appear to be determined solely by decreased Cd accumulation, but is associated with increased binding of testicular Cd to a MT-like protein. However, this increase is not accompanied by a proportional increase in the total Cd-binding capacity of the MT-like protein in A/J testes compared to 129 J testes.