The role of the antioxidant enzymes in erythrocytes in the development of arterial hypertension among humans exposed to lead.
The study population included employees of metal works, with significant exposure to lead (Pb) for about 20 years (mean blood lead level PbB = 43 microg/dl), divided into four groups: normotensive (Pb-normotensive), high-normotensive, first (HT-1), and second degree (HT-2) of hypertension. The control group comprised of 30 office workers with normal blood pressure and no history of occupational exposure to lead. In erythrocytes, the activity of antioxidant enzymes and lipid peroxidation (measured as concentration of malondialdehyde (MDA)) was estimated. MDA concentration, glutathione peroxide (GPx), and superoxide dimutase (SOD) activities were significantly higher in Pb-normotensive group when compared to the normotensive control. Body mass index, age, duration of exposure to lead, and PbB were higher in both hypertensive groups than in Pb-normotensive or high-normotensive groups. MDA increased in HT-1 group by 48% and in HT-2 by 72%, and the activity of GPx decreased significantly in HT-1 group, by 30% and in HT-2 by 43%. No significant differences were observed in their activity of SOD, catalase, and glutathione reductase in erythrocytes. Arterial blood pressure (both systolic and diastolic) positively correlated with body mass index (BMI), age, lead exposure duration, PbB, MDA, and negatively correlated with GPx. There was no significant correlation between BMI and MDA, BMI and GPx, age and MDA, AND age and GPx.


CONCLUSIONS
(1) lead increases erythrocyte MDA concentration and the activity of GPx as well as SOD in normotensive subjects. (2) Among individuals exposed to lead, with arterial hypertension diagnosed, higher body mass index, age, values of blood lead level, and prolonged exposure to lead have been noticed, accompanied by intensified oxidative stress and the decrease in the activity of glutathione peroxidase in erythrocytes. The reasons for increase of blood pressure in lead exposure remain unrecognized.
Kasperczyk
Sławomir
S
Department of Biochemistry in Zabrze, Medical University of Silesia, Katowice, Poland. kaslav@mediclub.pl
Kasperczyk
Janusz
J
Ostałowska
Alina
A
Zalejska-Fiolka
Jolanta
J
Wielkoszyński
Tomasz
T
Swietochowska
Elzbieta
E
Birkner
Ewa
E
D000328:Adult; D000975:Antioxidants / Q000032:analysis; D002374:Catalase / Q000032:analysis / Q000378:metabolism; D004912:Erythrocytes / Q000201:enzymology*; D005979:Glutathione Peroxidase / Q000032:analysis; D005980:Glutathione Reductase / Q000032:analysis / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000201:enzymology / Q000209:etiology*; D007854:Lead / Q000097:blood / Q000633:toxicity*; D007855:Lead Poisoning / Q000097:blood / Q000150:complications / Q000201:enzymology*; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D016273:Occupational Exposure; D011524:Protoporphyrins / Q000097:blood; D013482:Superoxide Dismutase / Q000032:analysis / Q000378:metabolism
D000975:Antioxidants; D011524:Protoporphyrins; C017803:zinc protoporphyrin; D007854:Lead; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase