Comparative analysis of antioxidants against cadmium induced reproductive toxicity in adult male rats

Abstract

The present study was conducted to compare and evaluate the potential benefits of three different antioxidants in reversing cadmium (Cd)-induced reproductive toxicity in adult male rats. Rats (n ¼ 5) weighing 180 AE 20 gm were divided into five groups (control, Cd, Cd þ sulforaphane, Cd þ vitamin E, and Cd þ plant extract). Treated groups received CdCl 2 (0.2 mg/kg), sulforaphane (25 mg/rat), vitamin E (75 mg/kg), and plant extract (100 mg/kg) for 15 days. Blood samples and testicular tissues were obtained for estimation of testosterone, Zn, and Cd concentration and daily sperm production/efficiency of sperm production. Cadmium exposure caused a significant decrease in final body weight (p50.0001). The plasma concentrations of Cd were significantly increased and Zn concentration decreased (p50.0001) in the Cd group as compared to the control group. The testicular concentrations of Cd were significantly increased and Zn concentration decreased (p50.0001) in the Cd group as compared to the control group. Cadmium exposure caused a significant decrease (p50.0001) in plasma testosterone concentrations and daily sperm production as compared to the control group. More significant effects were observed with Cdþsulforaphane, Cd þ vitamin E, and Cd þ plant extract treated groups in slashing Cd-induced toxicity. Present findings suggest that Ficus religiosa and sulforaphane are more powerful antioxidants as compared to vitamin E in reversing the oxidative stress and can have a protective role against Cd induced reproductive toxicity in adult male rats. Part of the mechanism involved in this protective role seems to be associated with the antioxidant properties of these agents in reducing reproductive damage.

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

“…As expected, Cd treatment decreased sperm motility and sperm number both in the cauda epididymides and testes, DSP/gm testis and serum testosterone level and increased abnormal sperm morphology (Jahan et al., ; Pires et al., ). The co‐treatment with EtOH increased further the number of abnormal spermatozoa and cauda epididymal sperm numbers, and there was also increased tendency for sperm motility, sperm numbers in the testes and DSP/gm testis to be modified in the Cd+EtOH‐treated animals.…”

“…EtOH was administered as 50% solution, and the volume administered to each animal corresponds to a dose of 5 g/kg body weight which has been reported to induce oxidative tissue damage in rats (Jurczuk et al., ), and correspond to the exposure that may take place in human life (Brzóska et al., ; Jurczuk, Brzo′ska, & Moniuszko‐Jakoniuk, ). We choose 15 days for three reasons: it is the period which Cd at 50 mg/kg body weight administered via the oral route increased lipid peroxidation in the testis of the rats ( our preliminary findings ), as well as the reports of others were Cd‐administered subcutaneously for 15 days to rats, at a dose much lower than was used in this study impaired sperm production and decreased testosterone level (Jahan, Khan, Ahmed, & Ullah, ), and thirdly, the duration of the spermatogenic cycle in rat is 12.5 days (Aslam et al., ; Gonzales, Nieto, Rubio, & Gasco, ). It would therefore be interesting to know early effects of Cd+EtOH mixtures on sperm quality, and spermatogenesis.…”

“…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, ).…”

Role of low exposure to metals as male reproductive toxicants

“…Our research finding added evidence that low exposure to Cd in the general population could link to decreased sperm quality, particularly in viability. Literature on the subject has reported likely biological mechanisms, including altering homeostasis of reproductive hormones via the steroidogenic pathway and oxidative stress due to a decrease in the ability of sulfhydryl molecules to scavenge reactive oxygen species (Jahan et al, 2014; Ren et al, 2012). …”

Pharmacology of Ficus religiosa- A review

“…Cadmium exposure caused a significant decrease (p < 0.0001) in plasma testosterone concentrations and daily sperm production as compared to the control group. A significant effects were observed with Cd+ sulforaphane, Cd + vitamin E, and Cd + plant extract treated groups in slashing Cd-induced toxicity [120].…”