Subacute Testicular Toxicity to Cadmium Exposure Intraperitoneally and Orally.

The toxic effects of cadmium (Cd) on reproductive parameters are widely described in the literature. Experimental models often make use of the intraperitoneal route (i.p.), although human intoxication occurs preferentially by the oral route and can be continuous. However, little is known about the effect of Cd administration routes on the testicular structure. Thus, this study investigated the testicular impact of Cd exposure comparing both i.p. and oral routes, both single dose (SD), in addition to the oral route in fractional doses (FD). Swiss adult male mice received CdCl2 1.5 mg/kg i.p., 30 mg/kg oral SD, and 4.28 mg/kg oral FD for 7 consecutive days. The Cd bioaccumulation was observed in all routes, mainly in the oral FD route. The concentrations of testicular Ca and Cu decreased in all animals exposed to Cd, while Zn and Mn decreased only in the i.p. route. Testicular SOD activity was reduced in both routes of oral administration, while CAT increased in the i.p. route, and GST increased in all animals exposed to Cd. Changes in the tubular parameters and cell viability were observed in both routes of Cd administration but were more intense in the oral route, mainly in the FD. Serum testosterone concentration was reduced in both routes of oral administration. Tubular damage, such as the vacuolization of the seminiferous epithelium, germ cell detachment, and seminiferous tubule degeneration, occurred in all groups exposed to Cd. Therefore, the oral Cd administration presented greater potential to promote testicular damage, mainly when the metal was given in a fractionated way.

How Bad Is Aluminum Exposure to Reproductive Parameters in Rats?

Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in human daily life without any known biological function. It is known that exposure to high concentrations of Al impacts negatively on serum testosterone levels, testicular histomorphometry, and sperm parameters; however, no information is available about the effects of low exposure levels on reproduction. International organizations have established the Al concentration tolerated in drinking water as 3.35 × 10-4 mg/kg. Therefore, we aimed to compare the effects of long-term exposure to low and high concentrations of Al on male reproductive functions, focusing on testis, epididymis, and sperm parameters. Adult Wistar rats were exposed to aluminum chloride (AlCl3) at 6.7 × 10-5, 3.35 × 10-4, 10, and 40 mg/kg for 112 days by gavage. Al-exposed animals presented low values of testis and epididymis weight, and serum testosterone levels when compared to controls. The stereology of Leydig cells, epididymis histomorphometry, sperm motility, and structural integrity of sperm membranes changed depending on the Al concentration. In regard to epididymis histomorphometry, the initial segment and caput regions were more affected by Al exposure than distal regions. Otherwise, the histology of testis and epididymis did not alter after the Al exposure, as well as sperm morphology. In summary, we concluded that the consequences of Al exposure at low levels were as negative as high levels on reproductive parameters, suggesting adverse impact on male fertility.

Aluminum: A potentially toxic metal with dose-dependent effects on cardiac bioaccumulation, mineral distribution, DNA oxidation and microstructural remodeling.

Large amounts of aluminum (Al) are found in wastewater from industrial bauxite mining, which is often responsible for the contamination of drinking water sources in urban and rural communities. Although this metal exhibits broad environmental distribution, its cardiac repercussions are poorly understood, making it difficult to establish diagnostic criteria in cases of Al intoxication. In the absence of clinical data, we used a preclinical model to investigate the impact of Al exposure on heart bioaccumulation, molecular oxidation, micromineral distribution, structural and ultrastructural remodeling of the cardiac tissue. Male Wistar rats were equally randomized into five groups: G1 = distilled water; and G2 to G5 = 0.02, 0.1, 50, and 200 mg/kg aluminum solution, respectively. After 120 days, the hearts were collected and subjected to mineral microanalysis, immunoenzymatic detection of 8-OHdG, as well as bright field, polarizing, scanning and transmission electron microscopy to estimate the extent of the cardiac remodeling and cardiomyocytes ultrastructure. Long-term Al exposure induced dose-dependent bioaccumulation, micromineral imbalance, genomic DNA oxidation, structural and ultrastructural abnormalities of the cardiac tissue, resulting in extensive parenchymal loss, stromal expansion, diffuse inflammatory infiltrate, increased glycoconjugate and collagen deposition, subversion and collapse of the collagen network, reduced myocardial vascularization index, mitochondrial swelling, sarcomere disorganization, myofilament dissociation, and fragmentation in cardiomyocytes. Our findings indicated that the heart was sensitive to Al-mediated toxicity, especially in animals treated with the three highest doses of Al. In response to Al-induced loss of the parenchyma, heart stroma exhibited a reactive and compensatory expansion, which, in combination with the increased distribution of thick myofibrils and degenerated mitochondria in cardiomyocytes, provides morphological evidence that cardiac tissue adaptations are not enough to adjust the relationships between the parenchyma and stroma until a steady state is reached, resulting in continuous pathological remodeling potentially associated with Al-induced proinflammatory and pro-oxidant events.