The aim of this study was to estimate the activity of superoxide dismutase (SOD) and catalase in erythrocytes and malondialdehyde (MDA) in plasma of battery manufacturing workers (BMW) of Western Maharashtra (India) who were occupationally exposed to lead (Pb) over a long period of time (about 15 years). This study was also aimed to determine the Pb intoxication resulted in a disturbance of heme biosynthesis in BMW group. The blood Pb level of BMW group (n = 28) was found to be in the range of 25.8 – 78.0 μg/dL (mean + SD, 53.63 + 16.98) whereas in Pb unexposed control group (n = 35) the range was 2.8 – 22.0 μg/dL (mean + SD, 12.52 + 4.08). The blood level (Pb-B) and urinary lead level (Pb-U) were significantly increased in BMW group as compared to unexposed control. Though activated d- aminolevulinic acid dehydratase (ALAD) activities in BMW group did not show any significant change when compared to control group but activated / non activated erythrocyte – ALAD activities in BMW group showed a significant increase. Erythrocyte- zinc protoporphyrin (ZPP), urinary daminolevulinic acid (ALA-U) and porphobilinogen (PBG-U) of BMW groups elevated significantly as compared to control. A positive correlation (r = 0.66, p< 0.001) between Pb-B and ALA-U were found in BMW group but no such significant correlation (r = 0.02, p> 1.0) were observed in control group. Hematological study revealed a significant decrease of hemoglobin concentration, packed cell volume (%) and other blood indices and a significant increase of total leucocytes count in BMW group in comparison to control group. The serum MDA content was significantly increased (p< 0.001) and the activities of antioxidant enzymes such as erythrocyte- SOD (p< 0.001) and erythrocytecatalase (p< 0.001) were significantly reduced in BMW group as compared to control group. A positive correlation (r = 0.45, p<0.02) between Pb-B and serum MDA level was observed in BMW group (Pb-B range 25.8 – 78.0 μg / dL) but such significant correlation did not notice in control group (Pb-B range 2.8 – 22.0 μg / dL).The study clearly showed an adverse effect of heme biosynthesis and imbalance of pro-oxidant / antioxidant status in lead exposed battery manufacturing workers resulting in increase in lipid peroxidation associated with decrease in erythrocyte-SOD and erythrocyte-catalase activities.

Background: Nickel activates the signaling pathways through the oxygen sensing mechanism and the signaling cascades that control hypoxia-inducible transcriptional gene expressions through oxidative stress. This review emphasizes on the recent updates of nickel toxicities on oxidant and antioxidant balance, molecular interaction of nickel and its signal transduction through low oxygen microenvironment in the in-vivo physiological system.Discussion: ickel alters intracellular chemical microenvironment by increasing ionized calcium concentration, lipid peroxidation, cyclooxygenase, constitutive nitric oxide synthase, leukotriene B4, prostaglandin E2, interleukins, tumor necrosis factor-α, caspases, complement activation, heat shock protein 70 kDa and hypoxia-inducible factor-1α. The oxidative stress induced by nickel is responsible for the progression of metastasis. It has been observed that nickel exposure induces the generation of reactive oxygen species which leads to the increased expression of p53, NF-kβ, AP-1, and MAPK. Ascorbic acid (vitamin C) prevents lipid peroxidation, oxidation of low-density lipoproteins and advanced oxidation protein products. The mechanism involves that vitamin C is capable of reducing ferric iron to ferrous iron in the duodenum, thus the availability of divalent ferrous ion increases which competes with nickel (a divalent cation itself) and reduces its intestinal absorption and nickel toxicities.Conclusion: Reports suggested the capability of ascorbic acid as a regulatory factor to influence gene expression, apoptosis and other cellular functions of the living system exposed to heavy metals, including nickel.

We studied liver and kidney function tests of occupational lead exposed Battery Manufacturing Workers (BMW) (n = 30), Silver Jewelry Workers (SJW) (n = 30), and Spray Painters (SP) (n = 35) and normal healthy subjects (n = 35), all 20 to 40 years of age, in Western Maharashtra (India). Venous blood and random urine samples were collected from all groups. The blood lead (Pb-B) and urinary lead (Pb-U) levels were significantly increased in all experimental groups, except urinary lead excretion in SJW as compared with the controls. Liver functions tests parameters (serum transaminase enzymes SGOT, AST, SGPT, ALT) activities were significantly increased only in SP; no alteration was noticed in BMW and SJW as compared with the control group. Serum total protein levels were significantly decreased in all three experimental groups as compared with control subjects. Serum albumin concentrations were significantly decreased in SJW, SP, and increased in BMW. The serum globulin levels, however, were significantly decreased, and the albumin/globulin (A/G) ratio was increased in BMW and SJW as compared with the control. The bilirubin level was significantly increased only in BMW. Blood urea was significantly increased only in BMW, and blood urea and serum uric acid were decreased in SJW. The serum creatinine level was not significantly altered in any experimental groups. Increased Pb-B values in all experimental groups indicate the greater rate of lead absorption and impairment of liver and kidney functions in all three types of occupational lead-exposed workers of Western Maharashtra (India).