ascorbic-acid and cadmium-acetate

This study investigated the effects of gestational and lactational exposure to lead and cadmium on testicular steroidogenesis, antioxidant system and male accessory gland functions in F1 generation rats to understand the biochemical mechanisms involved in endocrine disruptions. Pregnant rats were subcutaneously administered with 0.05 mg kg(-1) body wt\\ day(-1) of sodium acetate (control), lead acetate, cadmium acetate and (lead acetate + cadmium acetate) throughout the gestational-lactational period, and all animals from each of the experimental groups were sacrificed by decapitation on post-natal day 56 for performing various biochemical assays. We observed significant reduction in the activities of testicular key steroidogenic enzymes and serum testosterone concentration along with significant depletion in cholesterol, ascorbic acid and reduced glutathione contents in all the metal-treated groups. Reductions in the activities of catalase and superoxide dismutase with concomitant increase in the levels of thiobarbituric acid reactive substance were observed in experimental groups. Both sperm contents and sperm motility patterns were significantly altered in all the metal-treated groups, suggesting the direct/indirect spermotoxic effects of lead and cadmium. The inhibitory effects of lead, cadmium and combined exposure on testicular steroidogenesis machinery, along with the male accessory gland functions, are indicative of multiple targets of lead and cadmium to disrupt male reproductive functions.

Topics: 17-Hydroxysteroid Dehydrogenases; Acetates; Animals; Antioxidants; Ascorbic Acid; Cadmium; Catalase; Cell Survival; Epididymis; Female; Lactation; Lead; Lipid Peroxidation; Male; Organometallic Compounds; Pregnancy; Rats; Reproduction; Sperm Count; Sperm Motility; Spermatozoa; Steroids; Superoxide Dismutase; Testis; Testosterone

In vitro generation of thiobarbituric acid reactive substances (TBARS) is frequently used to assess organ susceptibility to lipid peroxidation. The yield of TBARS is severalfold enhanced by an addition of iron ions with reductors or chelators such as ascorbate, NADPH, ADP or pyrophosphate. The process cannot be interpreted in a simple way, since it involves several enzymatic and nonenzymatic reactions. There are no clear interpretations of the ambiguous effects of denaturating factors and chelating agents on TBARS generation. Also controversy arises from the curvilinear relationship between the homogenate concentration and the yield of TBARS. This has been modelled in the present work by combining two functions describing the sequential reaction with two limiting steps. One of them is related to catalytic action of iron and ascorbate, while the other to an enzyme, possibly phospholipase A2, as has been suggested by some investigators. Two models should be considered since it is impossible to decide which kinetic equation should predominate in the model. Nevertheless, the model reflects kinetic properties of the process. The effects of catalyst concentration and some other modification upon the yield of TBARS were also investigated experimentally. The results of experiments and modelling showed that the analytical procedures used by investigators need standardisation as the results obtained under a variety of procedures may reflect quite different properties of the living systems.

Topics: Acetates; Animals; Ascorbic Acid; Brain; Cadmium; In Vitro Techniques; Iron; Kidney; Kinetics; Lipid Peroxidation; Liver; Models, Biological; Rats; Sodium Selenite; Thiobarbiturates; Thiobarbituric Acid Reactive Substances; Vitamin E