Protective role of pectin against cadmium-induced testicular toxicity and oxidative stress in rats

Abstract

Cadmium has been classified as an environmental pollutant and human carcinogen. Pectin is a family of complex polysaccharides that function as hydrating agents and cementing materials for the cellulosic network. The aim of this study was to evaluate the protective role of pectin against cadmium-induced testicular toxicity and oxidative stress in rats. Forty male Wistar rats were divided into five equal groups. Groups 1 and 2 were injected intraperitoneally (i.p.) saline (1 mg/kg) and pectin (50 mg/kg), respectively, two days/weeks over three weeks period. Groups 3-5 were injected i.p. with 1 mg/kg cadmium two days/week while groups 4 and 5 co-administrated i.p. with 25 and 50 mg/kg pectin, respectively, three days/week over three weeks period. The results of the present work revealed that cadmium-exposed rats showed decrease in serum testosterone, dehydroepiandrosterone sulfate and lactate dehydrogenase. Testicular cholesterol, total protein, glucose-6-phosphate dehydrogenase, 3β-hydroxysteroid dehydrogenase, superoxide dismutase, glutathione peroxidase, catalase, glutathione S-transferase and reduced glutathione levels were also decreased while testicular malondialdehyde level was increased after cadmium injection. On the other hand, serum luteinizing hormone, follicle stimulating hormone, sex hormone binding globulin and γ-glutamyl transpeptidase were increased after cadmium exposure. Cadmium also induced sperms loss. Co-administration of pectin with cadmium restores all the above parameters and sperms to the normal levels where pectin at higher dose was more effective than lower one. These results were supported by histochemical investigations. In conclusion, pectin can counteract the testicular toxicity and oxidative stress induced by cadmium and the effect was dose-dependent.

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

“…Because the lipid peroxidation level was higher in the testes of Cd+EtOH‐treated animals than in the Cd‐treated rats, the antioxidant defence systems in the testes of these animals were much more disturbed compared to the Cd‐treated animals, but the testicular antioxidant defence system of the testis of these animals was able to cope with the altered oxidative balance and could not allow further peroxidative changes. It is usually reported that GSH level decreased after Cd treatment (Arafa, Mohammad, & Atteia, ; Jahan et al., ; Kheradmand, Alirezaei, & Dezfoulian, ; Koriem, Fathi, Salem, Akram, & Gamil, ; Pires et al., ). However, contrary results have observed that low Cd concentration increased GSH level, whereas high Cd concentration depleted GSH level (Gaubin et al., ), suggesting a relationship between tissue concentration of GSH and Cd (Thomas, Wofford, & Neff, ; Vogiatzis & Loumbourdis, ).…”

Review of polyphenol‐rich products as potential protective and therapeutic factors against cadmium hepatotoxicity

“…Moreover, some essential bioelements such as Ca, Fe, Mg and Zn may decrease liver accumulation of Cd by diminishing its absorption and availability for hepatocytes (Boujelben et al, ; Matović et al, ; Rogalska et al, ; Ryu et al, ; Sarić et al, ). In reference to the fact that the major mechanism of hepatotoxic action of Cd is its ability to generate FR and ROS, literature sources notably emphasize the possibility of using substances that may increase the antioxidative potential of hepatocytes and combat the adverse effects of Cd‐induced oxidative stress at the cellular level such as polyphenolic compounds, vitamins C and E, carotenoids, minerals, tannins, pectin and coenzyme Q10 (Figure ) (Brzóska, Borowska, & Tomczyk, ; Brzóska, Rogalska, et al, ; El‐Sayed et al, ; Gong et al, ; Koriem, Fathi, Salem, Akram, & Gamil, ; Mężyńska et al, ; Ognjanović et al, ; Winiarska‐Mieczan, ).…”

“…Tannic acid was shown to prevent bones from Cd injury (Tomaszewska et al, 2017) and decrease the accumulation of this metal in the brain (Winiarska-Mieczan, 2013). The administration of pectin to rats improved the levels of antioxidants, decreased the concentration of MDA and ameliorated Cd-induced histopathological changes in the testes (Koriem et al, 2013). Moreover, owing to the chelating properties of dietary fiber (Borycka, 2012;Persson, Nyman, Liljeberg, Önning, & Frølich, 1991) consumption of fiber-rich food may also contribute to alleviate hepatotoxicity of Cd by decreasing gastrointestinal absorption of this metal and enhancing its elimination from the organism (Berglund et al, 1994).…”

“…sources notably emphasize the possibility of using substances that may increase the antioxidative potential of hepatocytes and combat the adverse effects of Cd-induced oxidative stress at the cellular level such as polyphenolic compounds, vitamins C and E, carotenoids, minerals, tannins, pectin and coenzyme Q10 (Figure 4)(Brzóska, Borowska, & Tomczyk, 2016;Brzóska, Rogalska, et al, 2015;El-Sayed et al, 2016;Gong et al, 2014;Koriem, Fathi, Salem, Akram, & Gamil, 2013;Mężyńska et al, 2016;Ognjanović et al, 2006;Winiarska-Mieczan, 2013).So far, data on the beneficial effect of compounds of plant origin regarding the effect of Cd on the liver have derived mainly from animal models and in vitro studies. However, the well-established effectiveness of these products in the prevention and therapy of various diseases in humans(Boncheva, Georgiev, & Shishov, 2013;Bozzetto et al, 2015;Chang, Peng, Yeh, Kao, & Wang, 2014;Henning et al, 2015;Hokayem et al, 2013;Ni et al, 2017;Pezeshki, Safi, Feizi, Askari, & Karami, 2016;Rasines-Perea & Teissedre, 2017;Soleimani, Paknahad, Askari, Iraj, & Feizi, 2016;Tresserra-Rimbau et al, 2014;Venancio et al, 2017) allows to suppose that these plant ingredients may also be effective in the prevention and treatment of liver injury caused by this toxic metal.…”

The Protective Effect of Omega-3 Oil against Cadmium Chloride Induced Nephrotoxicity in Rat

“…Cd can also induce hematological and biochemical toxicity [9], hepatotoxicity [45], nephrotoxicity [41,42], neurotoxicity [44] and testotoxicity [24,30]. Furthermore, Cd can induce several toxic effects in newly born rat pups on lactational exposure [13].…”