Effect of Physalis peruviana L. on Cadmium-Induced Testicular Toxicity in Rats

Abstract

Cadmium (Cd) stimulates the production of reactive oxygen species and causes tissue damage. We investigated here the protective effect of Physalis peruviana L. (family Solanaceae) against cadmium-induced testes toxicity in rats. Twenty-eight Wistar albino rats were used. They were divided into four groups (n=7). Group 1 was used as control. Group 2 was intraperitoneally injected with 6.5 mg/kg body weight (bwt) of cadmium chloride for 5 days. Group 3 was orally treated with 200 mg/kg bwt of methanolic extract of physalis (MEPh). Group 4 was pretreated with MEPh before cadmium for 5 days. Changes in body and testes weights were determined. Oxidative stress markers, antioxidant enzymes, and testosterone level were measured. Histopathological changes of testes were examined, and the immunohistochemical staining for the proapoptotic (caspase-3) protein was performed. The injection of cadmium caused a significant decrease in body weight, while a significant increase in testes weight and testes weight index was observed. Pretreatment with MEPh was associated with significant reduction in the toxic effects of Cd as shown by reduced testicular levels of malondialdehyde, nitric oxide, and caspase-3 expression and increased glutathione content, and the activities of superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, and testosterone were also increased. Testicular histopathology showed that Cd produced an extensive germ cell apoptosis, and the pretreatment of MEPh in Cd-treated rats significantly reduced Cd-induced testicular damage. On the basis of the above results, it can be hypothesized that P. peruviana L. has a protective effect against cadmium-induced testicular oxidative stress and apoptosis in the rat.

Rutin, an antioxidant flavonoid, induces glutathione and glutathione peroxidase activities to protect against ethanol effects in cadmium-induced oxidative stress in the testis of adult rats

“…Histopathological changes in testis tissue were observed when the Cd dose was higher (Bomhard et al., ; Jiang et al., ). Doses of Cd lower than was used in the present study were reported previously to induce pathological changes only when administered intraperitoneally or subcutaneously for few hours or few days in rodents (Ige et al., ; Kheradmand et al., ; Minutoli et al., ; Othman, Nada, Zaki, & Abdel Moneim, ) or when administered orally for a longer time (90‐days; El‐Refaiy & Eissa, ; 8‐weeks; Sakr & Nooh, ). In most of these studies, the testicular Cd contents increased from 1.22 to 176 μg/g (Arafa et al., ; Jahan et al., ; Koriem et al., ) depending on the duration of treatment.…”

The Protective Properties of the Strawberry (Fragaria ananassa) against Carbon Tetrachloride-Induced Hepatotoxicity in Rats Mediated by Anti-Apoptotic and Upregulation of Antioxidant Genes Expression Effects

“…In recent years, considerable clinical and experimental data has revealed that oxidative stress is caused by an imbalance between the oxidant and antioxidant systems within the body (Ghatak et al, 2011 ). There is a great deal of evidence indicating that natural substances from edible and medicinal plants exhibit strong antioxidant activity that could act against hepatic toxicity caused by various toxicants (Othman et al, 2014 ). One of those candidate plants is strawberry.…”

Protective effects of Vitamin E on CCl4-induced testicular toxicity in male rats

“…Spermatogenesis is orchestrated by two main regulations: endocrine [luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from pituitary gland] and local intercellular communications mediated by a complex interplay of hormones and testicular growth factors, among which testosterone is crucial for testicular functioning (3). Recent studies concluded that oxidative stress, exhibited by exposure to toxic chemicals, causes a major damage to sperm quality by disrupting the anti-oxidant and reactive oxygen species (ROS) balance and thus resulting in abnormalities of spermatogenesis and male infertility (22,32).…”