Co-exposure to Aluminium and Cadmium Mediates Postpartum Maternal Variation in Brain Architecture and Behaviour of Mice; Involvement of Oxido-nitrergic and Cholinergic Mechanisms : Postpartum effects of Aluminium and Cadmium co-exposure in pregnancy.

Most research has not been done on the possible relationship between pregnant women's cross-metal exposures and postpartum neuroendocrine functions. The purpose of this study was to look into how co-exposure to aluminium chloride (AlCl3) and cadmium chloride (CdCl2) affected the neuroendocrine and neurometabolic changes in postpartum mice. A total of 24 adult pregnant female mice were used for the study. Group 1 served as control and received neither AlCl3 nor CdCl2 (n=6), group 2 comprised pregnant mice treated with AlCl3 (10mg/kg), group 3 with CdCl2 (1.5mg/kg), group 4 with a combination of AlCl3 (10 mg/kg) and CdCl2 (1.5 mg/kg).Oral treatment of animals was done daily from gestation day 7 to gestation day 20. Upon delivery and weaning on postnatal day 21 (PND 21), behavioural assessment was done on the postpartum mice and immediately followed by sacrifice for assessment of histological and neuroendocrine markers. Our findings revealed that the brain-to-body weight ratio was affected and brain oxidative stress was elevated in mice exposed to AlCl3 and CdCl2 during pregnancy. Given the strong association between postpartum hyperactivity, social interaction index, brain catalase and acetylcholinesterase activity, and the brain/body weight ratio, it is plausible that these effects have played a role in the adverse behavioural abnormalities observed in the postpartum maternal mice. Moreover, it was noted that in certain situations, co-exposures to the metals tended to have opposite effects to single metal exposures.

Prenatal double-hit with aluminium and cadmium mediate testicular atrophy and hypothalamic hypoplasia: the role of oxido-nitrergic stress and endocrine perturbations.

There is limited experimental evidence on the biochemical consequences of aluminium (Al) and cadmium (Cd) co-exposures during pregnancy and postnatal life.This study investigated the impacts of perinatal Al chloride (AlCl3) and Cd chloride (CdCl2) co-exposures on neuroendocrine functions in mice offspring during postnatal life. The study comprised of four pregnant experimental groups. Group 1 received AlCl3 (10 mg/kg), group 2 were administered CdCl2 (1.5 mg/kg), while group 3 received both AlCl3 (10 mg/kg) and CdCl2 (1.5 mg/kg) (AlCl3+CdCl2), and group 4 received saline (10 mL/kg) only and served as control group. All experimental animals were chemically exposed once daily from gestation days 7-20. Upon delivery, male pups were regrouped based on maternal chemical exposure on postnatal day 21 (PND 21) and allowed to grow to adulthood until PND 78, after which they were sacrificed for assessment of neuroendocrine markers and histological investigations. There was no statistical significance (p > 0.05) on follicle stimulating hormone, testosterone, estrogen and progesterone, thyroid stimulating hormone, thyroxine (T4) in all treatment groups relative to controls|. However, AlCl3 and AlCl3-CdCl2 significantly (p < 0.05) reduced triiodothyronine (T3) levels, with a profound increase in T3:T4 ratio by AlCl3, and AlCl3+CdCl2 compared to control. Furthermore, pups from pregnant mice treated with CdCl2 and AlCl3+CdCl2 demonstrated increased testicular malondialdehyde concentration with increased catalase activity relative to controls, suggesting oxidative imbalance. In addition, AlCl3, CdCl2, and AlCl3+CdCl2 exposures induced testicular and hypothalamic architectural disruption compared to controls, with marked architectural derangement in the AlCl3+CdCl2 group. Our findings suggest that prenatal co-exposures to Alcl3 and CdCl2 induce testicular and hypothalamic alterations in offspring via a testicular oxidative stress and thyrotoxicosis-dependent mechanisms.

Hepatocellular degeneration in mice co-exposed to in-utero aluminium and cadmium: Implication of a disordered antioxidant and energy homeostatic response in the liver.

The current study comprised four groups of pregnant animals viz; Control (CTR) received 10 ml/kg of normal saline, Al:10 mg/kg of AlCl3, Cd: 1.5 mg/Kg of CdCl2 Al+Cd; 10 mg/kg of AlCl3 and 1.5 mg/Kg of CdCl2. Treatment was done from pregnancy days (PNT) 7-20. After delivery, male animals were weaned on PSD 21 and sacrificed on PSD 78. From the study significant increases on serum liver enzymes in the group exposed to Cd and that exposed to Al+Cd were observed. The study further showed altered serum and hepatic antioxidant balance for the Cd, Al and Al+Cd groups compared to control. Similarly, lactate dehydrogenase (LDH) and succinate dehydrogenase (SDH) activities in the liver were elevated in Cd and Al+Cd groups while an altered liver histological feature in treated groups were also observed. it was concluded that in utero co-exposure to Al and Cd had the ability to alter hepatic functional indices.

Influence of farmyard manure on some morphological and biochemical parameters of cowpea (Vigna unguiculata) seedling grown in cadmium-treated soil.

The present study aims to assess the effects of the two kinds of farmyard manure (poultry and pig manures) as amendments for soil on cadmium (Cd) toxicity in plants using cowpea seedlings as plant model. Cd toxicity was evaluated by assessing the effect of the metal on the growth rate and antioxidant status as well as the ability of the plant to metabolise xenobiotic. There was a significantly (p < 0.05) increased concentration of Cd in the root, stem and leaves of cowpea seedlings grown in all the treated soils relative to control. Addition of poultry manure to the soil significantly (p < 0.05) decreased the level of Cd in these component parts of the seedlings and their corresponding bioaccumulation factor in a dose-dependent manner as compared with treatments with Cd pollution without manure addition and Cd pollution with pig manure addition. There was restoration of Cd-induced effect on growth rate parameters to levels comparable to controls in cowpea seedlings grown in Cd-treated soil augmented with poultry manure but not in cowpea seedlings in cadmium-treated soil with pig manure amendments. Similarly, augmentation of Cd-treated soil with pig manure did not alter the Cd-induced effect on the levels of superoxide dismutase (SOD) and lipid peroxidation (LPO) in leaf, stem and roots, as SOD remained significantly (p < 0.05) decreased and LPO increased relative to control. On the other hand, the levels of SOD and LPO in these parts of cowpea seedlings grown in Cd-treated soils amended with poultry manure were restored to a level not significantly (p > 0.05) different from control. Like in the case of SOD, the Cd-induced inhibition of the activity of xenobiotic metabolising enzymes, aldehyde oxidase and sulphite oxidase remained significantly (p < 0.05) decreased in the organs of seedling grown in Cd-treated soil amended with pig manure. Conversely, the Cd-induced effect on the activities of these enzymes was reversed in the organs of seedlings exposed to Cd and poultry manure as it was not significantly (p > 0.05) different from control. In conclusion, the findings of the study revealed that supplementation of Cd-treated soils with pig and poultry manures reversed effects of Cd on cowpea seedlings. However, poultry manure was more effective than pig manure in ameliorating the effects of Cd.

Comparative effect of water and food-chain mediated cadmium exposure in rats.

This study sets out to compare the absorption and toxicity of Cadmium (Cd) administered via the food-chain and inorganic Cd administered in drinking water after 1 and 3 months exposure using rats as animal model. The food-chain was mimicked by exposing rats to diet containing Cd pre-exposed fish. The uptake of Cd by the rats after both mode of exposure was calculated by summing up the Cd burden in the liver and kidneys and was expressed in terms of % intake. The toxicity of Cd was assessed by monitoring biochemical indices of liver function in the plasma and liver. Regardless of the mode of exposure of the rats, the Cd load in the liver and kidney was significantly (P < 0.05) higher than the respective controls with the kidney having a significantly higher load than the liver after both periods of exposure. However irrespective of the mode of exposure, more Cd was accumulated in the liver and kidney of the 3 months exposed rats relative to those exposed for 1 month. The uptake of Cd by rats exposed to Cd via the food-chain for 1 and 3 months was significantly (P < 0.05) lower when compared to the corresponding water mediated Cd exposed rats, except for the liver after 3 months of exposure. The liver L-ALT activity of rats administered inorganic Cd in drinking water for 1 and 3 months was significantly (P < 0.05) lower as compared to controls. Parallel analysis of the plasma showed no significant (P > 0.05) difference in L-ALT activity between both groups after the same periods of exposure. The L-AST activity in the plasma of rats similarly exposed to Cd for 1 and 3 months was significantly (P < 0.05) higher as compared to controls with a corresponding reduction in the liver. Conversely no significant (P > 0.05) change was observed in plasma and liver L-ALT and L-AST activities after food-chain mediated exposure to Cd for 1 and 3 months in relation to their respective controls. These findings indicate that Cd incorporated in fish is more easily bioavailable, but less toxic relative to inorganic Cd salts at the end of 3 months of exposure in rats.