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Curcumin (diferuoyl methane) from turmeric is a well-known biologically active compound. It has been shown to ameliorate oxidative stress and it is considered to be a potent cancer chemopreventive agent. In our previous study the antioxidative effects of curcumin in cadmium exposed animals were demonstrated. Also manganese exerts protective effects in experimental cadmium intoxication. The present study examined the ability of the manganese complex of curcumin (Mn-curcumin) and curcumin to protect against oxidative damage and changes in trace element status in cadmium-intoxicated male mice. Curcumin or Mn-curcumin were administered at equimolar doses (0.14 mmol/kg b.w.) for 3 days, by gastric gavages, dispersed in methylcellulose. One hour after the last dose of antioxidants, cadmium chloride (33 micromol/kg) was administered subcutaneously. Both curcumin and Mn-curcumin prevented the increase of hepatic lipid peroxidation -- expressed as MDA level, induced by cadmium intoxication and attenuated the Cd-induced decrease of hepatic GSH level. No change in hepatic glutathione peroxidase or catalase activities was found in Cd-exposed mice. A decreased GSH-Px activity was measured in curcumin and Mn-curcumin alone treated mice. Neither curcumin nor Mn-curcumin treatment influenced cadmium distribution in the tissues and did not correct the changes in the balance of essential elements caused by Cd-treatment. The treatment with Mn-curcumin increased the Fe and Mn content in the kidneys of both control and Cd-treated mice and Fe and Cu content in the brain of control mice. In conclusion, regarding the antioxidative action, introducing manganese into the curcumin molecule does not potentiate the studied effects of curcumin.

Oxidative tissue damage is considered an early sign of cadmium (Cd) toxicity and has been linked with carcinogenesis. Manganese(II)-at low doses, was found to act as a potent antioxidant against oxidative stress in different in vitro systems producing lipid peroxidation conditions. The present study investigates in vivo antioxidant effects of Mn2+ pretreatment in acute Cd intoxication with regard to lipid peroxidation, antioxidant defense system and cadmium distribution in the tissues of mice. Four groups of male mice (n=7–8) were used: Cd group was injected sc a single dose of CdCl2 · 2½ H2O · (7 mg/kg b.w.); Cd+Mn group was treated ip with MnCl2 · 4H2O (20 mg/kg b.w.) 24 hours before Cd intoxication; Mn group received manganese treatment only; Control group received saline only. Twenty-four hours after Cd intoxication an increased lipid peroxidation (p<0.05), depleted GSH level (p<0.01), increased activity of GSH-Px (p<0.05) and inhibited CAT activity (p<0.01) were found in Cd-treated group compared to controls. Manganese(II) pre-treatment either completely prevented (LP, GSH, GSH-Px) or significantly attenuated (CAT) these changes. Manganese(II) treatment alone decreased LP, enhanced hepatic GSH level and had no effect on antioxidant enzymes compared to control group. A significant increase of Cd concentration in the liver and decreased Cd concentration in the kidneys and testes were found in Cd+Mn treated mice compared to Cd-only treated group. The effect of manganese may result from a different metallothionein induction in particular organs. Manganese(II) pretreatment attenuated the interference of cadmium with Ca homeostasis, the alteration in Zn and Cu levels remained mostly unaffected.

The influence of melatonin, curcumin, quercetin, and resveratrol pretreatment on ferric nitrilotriacetate (Fe-NTA)-induced oxidative renal damage was studied. Male Wistar rats were treated orally once daily for 3 days with melatonin (10 mg/kg), curcumin (50 mg/kg), quercetin (15 mg/kg), and resveratrol (10 mg/kg). One hour after the last dose of antioxidants, a single dose of Fe-NTA was administered (8 mg of Fe/kg body weight, i.p.) to pre-treated animals. Twenty-four hours after Fe-NTA administration, the lipid peroxidation (LP), reduced glutathione (GSH), catalase (CAT), and glutathione peroxidase (GSH-Px) were estimated in kidney homogenates. Iron, zinc, and copper concentrations were estimated in kidney tissue. Administration of Fe-NTA to rats induced renal LP (170%, P < 0.001) and inhibited catalase (78%, P < 0.05) in the kidney. The oral pretreatment with melatonin, curcumin, quercetin, and resveratrol each one was effective in decreasing the Fe-NTA-induced LP ( P < 0.001); however, it did not influence the FeNTA-induced inhibition of renal CAT activity. No changes were found in renal GSH level and GSH-Px activity compared to control animals. The pretreatment with antioxidants did not affect the increase in renal iron content, blood urea nitrogen/creatinine ratio, and relative kidney weight of FeNTA-intoxicated rats. The results indicate that the pretreatment with natural antioxidants, curcumin, melatonin, quercetin, and resveratrol, significantly and equally suppressed lipid peroxidation induced by Fe-NTA but had no effect on other markers of FeNTA nephrotoxicity and iron deposition in kidneys.